Cryptococcal choroiditis is an uncommon fungal infection in which Cryptococcus neoformans or C. gattii—yeast-like fungi usually found in bird droppings and in certain trees—settle in the choroid, the blood-rich, oxygen-carrying layer that lies between the retina and the white outer coat (sclera) of the eye. When spores travel through the bloodstream (often after first infecting the lungs or central nervous system) they can seed the choroid, spark inflammation, trigger tiny pockets of pus-like material called granulomas, and disturb the delicate balance that keeps the retina nourished. Left untreated, the infection may extend forward into the retina, vitreous, or optic nerve, causing blurred vision or even permanent blindness. Because Cryptococcus thrives where immunity is weak, cryptococcal choroiditis often serves as an ophthalmic warning sign of advanced HIV/AIDS, prolonged high-dose steroid use, organ transplantation, or other immunosuppressive states.
Cryptococcal choroiditis is an infection and inflammation of the choroid (the vascular layer behind the retina) caused by the fungus Cryptococcus (usually Cryptococcus neoformans, less commonly C. gattii). It is not a primary eye disease but an ocular sign of a widespread systemic infection, most often seen in people whose immune systems are weak—particularly advanced HIV/AIDS, organ transplant recipients, or those on immune-suppressing drugs. The fungus reaches the eye through the bloodstream, and because the choroid has abundant blood supply, it can become seeded, forming creamy yellow lesions that can impair vision. Often, other signs of eye inflammation (like vitritis) are minimal because severe immunosuppression blunts the inflammatory response. Early recognition matters because this eye finding usually mirrors a serious underlying condition such as cryptococcal meningitis or disseminated cryptococcosis. EyeWiki EyeWiki
After inhalation, Cryptococcus reaches the lungs, hides inside macrophage “trojan horses,” and can enter the bloodstream. Its thick polysaccharide capsule helps it dodge normal immune surveillance. When the fungus reaches the eye, the high vascular flow of the choroid makes a perfect landing pad. Here, yeast cells multiply, release capsule fragments that block tiny blood vessels, and lure inflammatory cells that further clog choroidal circulation. Edema (fluid leak) and granuloma formation lift the overlying retina like little blisters; photoreceptors starve, and vision dims. If the infection is recognized early and treated promptly with antifungal drugs (such as amphotericin B and flucytosine followed by fluconazole), the lesions can shrink and vision may recover. If detection is late—or the immune system cannot cooperate—scars or atrophy can leave irreversible blind spots.
Types of Cryptococcal Choroiditis
Solitary Choroidal Granuloma – a single dome-shaped lesion often discovered incidentally in one eye during routine exam.
Multifocal Choroiditis – many small yellow-white patches scattered across the posterior pole or mid-periphery of both eyes.
Disseminated Ocular Cryptococcosis – choroiditis plus retinal infiltrates, vitreous haze, or optic disc swelling, reflecting a higher body fungal load.
Immune-Reconstitution Inflammatory Syndrome (IRIS)-associated Choroiditis – paradoxical worsening or new lesions after antiretroviral therapy revives immune activity in HIV patients.
Cryptococcal Chorioretinitis – infection spills from the choroid into retinal layers, sometimes mimicking viral retinitis.
Endogenous Endophthalmitis with Choroidal Foci – fulminant seeding of the entire eye cavity, often in septic shock; choroiditis is part of a global intra-ocular storm.
Each pattern signals a different balance between fungal virulence, host immunity, and treatment delay, which in turn steers management urgency and prognosis.
Main Causes
Below are the 20 most important underlying situations that make cryptococcal choroiditis possible. Each paragraph names the cause and explains how it paves the way for the fungus.
Advanced HIV-AIDS – A CD4 count below 100 cells/µL strips away T-cell surveillance, allowing Cryptococcus to spread from lung to blood to eye almost unopposed.
Solid-Organ Transplantation – Anti-rejection drugs such as tacrolimus, mycophenolate, and corticosteroids blunt cellular immunity and let latent spores awaken.
Hematopoietic Stem Cell Transplant – Neutropenia and prolonged immunosuppressants create a double hit, greatly increasing invasive fungal risk.
Prolonged High-Dose Corticosteroid Therapy – Steroids dampen macrophage function and cytokine signaling, giving encapsulated yeasts free rein.
Cirrhosis – Impaired liver complement production and portal hypertension lower systemic immune competence, increasing fungal translocation.
Chronic Kidney Disease on Dialysis – Repeated vascular access and uremia weakens both innate and adaptive immunity, opening a fungal doorway.
Sarcoidosis Under Immunosuppressive Agents – Disease-related T-cell dysfunction plus drugs like methotrexate increase susceptibility.
Rheumatoid Arthritis on Biologics – TNF-α inhibitors or JAK inhibitors reduce granuloma maintenance, an Achilles’ heel against encapsulated fungi.
Leukemia or Lymphoma – Malignant crowding of bone marrow diminishes normal leukocyte output; chemotherapy deepens the trough.
Diabetes Mellitus – High glucose dulls neutrophil chemotaxis and phagocytosis, allowing fungal bloodstream survival.
Chronic Lung Disease with Structural Damage – Bullae, bronchiectasis, or previous tuberculosis cavities serve as fungal nurseries that can hematogenously seed the eye.
Silicone Oil Tamponade or Intra-ocular Implants – Rarely, intra-ocular foreign material can harbor fungi, leading to secondary choroiditis.
Bird Guano or Eucalyptus Tree Exposure – Heavy environmental inoculation (pigeon farms, tree-cutting work) raises the fungal dose inhaled.
Travel to C. gattii-Endemic Regions – Regions such as Pacific Northwest or parts of Australia harbor more virulent strains that infect even immunocompetent hosts.
Pregnancy – Relative cell-mediated immune suppression during gestation mildly heightens risk in endemic areas.
Malnutrition – Protein-energy deficiency blunts lymphocyte proliferation, undermining antifungal defenses.
Chronic Alcohol Abuse – Ethanol impairs macrophage oxidative burst and micronutrient absorption, both critical in fungal killing.
Congenital T-cell–Mediated Immunodeficiencies – Rare disorders like DiGeorge syndrome create lifelong vulnerability to encapsulated yeasts.
Post-Traumatic Splenectomy – Loss of splenic filtration allows capsulated organisms such as Cryptococcus to persist in blood longer.
Idiopathic CD4 Lymphocytopenia – A puzzling, non-HIV low-CD4 state discovered incidentally can present first with cryptococcal ocular disease.
Common Symptoms
Gradually Blurring Central Vision – Early granulomas disturb macular photoreceptors, making reading or face recognition fuzzy.
Peripheral Blind Spots (Scotomas) – Multifocal lesions interrupt choroidal blood flow to localized retina areas, creating patchy shadows.
Floaters – If inflammation leaks cells into the vitreous, patients see moving specks or cobwebs.
Photopsia (Flashes of Light) – Retinal irritation produces transient flickers, especially in dark settings.
Reduced Contrast Sensitivity – Colors look dull and dim because the retina receives less oxygen.
Difficulty Seeing at Night (Nyctalopia) – Rod cells, starved of nutrients, struggle in low-light situations.
Metamorphopsia – Straight lines warp or bend when the retina is gently lifted by choroidal swelling.
Eye Pain Deep Inside – Rare but possible if inflammation reaches ciliary nerves or raises intra-ocular pressure.
Red Eye – Mild surface injection can accompany deeper infection, though often the external eye looks calm (“white-eye choroiditis”).
Tearing and Light Sensitivity – Secondary anterior segment inflammation makes sunlight harsh.
Headache – A clue to concurrent cryptococcal meningitis, which co-exists in many cases.
Nausea and Vomiting – Another meningitis sign; raised intracranial pressure and ocular pain can coexist.
General Fatigue – Systemic infection taxes energy and may coexist with fever or weight loss.
Double Vision – Cranial nerve palsy from meningitis plus ocular involvement can cause diplopia.
Sudden Vision Loss – A late, devastating sign when lesion hemorrhages or retinal detachment occurs.
Further Diagnostic Tests
A. Physical-Exam Based
Direct Ophthalmoscopy – Hand-held light reveals creamy yellow choroidal masses with fuzzy borders.
Dilated Fundus Examination with 90-D Lens – Slit-lamp biomicroscopy maps lesion size, depth, and retinal involvement.
Color Vision Plates (Ishihara) – Subtle macular dysfunction appears as new mistakes on color tests.
Amsler Grid Test – Patient marks warped lines, pinpointing macular metamorphopsia from overlying choroidal elevation.
B. Manual & Bedside Functional Tests
- Visual-Acuity Snellen Chart – Quantifies central vision loss and tracks recovery during treatment.
- Contrast-Sensitivity Pelli-Robson Chart – Detects early functional impairment even when Snellen remains good.
- Visual-Field Perimetry (Automated Humphrey or Manual Goldmann) – Maps scotomas, guiding lesion localization and therapeutic response.
C. Laboratory & Pathological Investigations
- Serum Cryptococcal Antigen (CrAg) Lateral Flow Assay – A rapid finger-stick test detecting capsular polysaccharide; high titers signal disseminated disease.
- CSF Analysis with India-Ink Stain & CrAg – Required if meningitis suspected; yeast cells show halo on microscopy.
- Blood Culture on Sabouraud Agar – Grows Cryptococcus in systemic sepsis or fever of unknown origin.
- Polymerase-Chain Reaction (PCR) for Cryptococcus DNA – Sensitive amplification confirming species, useful in low-antigen-titer cases.
- Histopathology of Choroidal Biopsy – Rarely performed; shows encapsulated budding yeasts within granulomas, highlighted by mucicarmine stain.
D. Electrodiagnostic Studies
- Full-Field Electroretinogram (ERG) – Reduced a-wave and b-wave amplitudes reflect photoreceptor and inner-retina dysfunction overlying choroiditis.
- Visual-Evoked Potentials (VEP) – Slowed P100 latency hints at optic-nerve involvement or retrobulbar demyelination secondary to infection.
E. Imaging Tests
- Optical Coherence Tomography (OCT) – High-resolution cross-sections show serous retinal detachment, hyper-reflective choroidal nodules, and sub-retinal fluid.
- Enhanced-Depth-Imaging OCT (EDI-OCT) – Quantifies choroidal thickness and offers clearer view of deeper nodules.
- Fundus Fluorescein Angiography (FFA) – Early hypofluorescence (blocked choroidal perfusion) followed by late leak around lesion edges.
- Indocyanine-Green Angiography (ICG) – Superior for choroidal circulation; lesions appear hypofluorescent in all phases, highlighting fungal foci.
- B-Scan Ocular Ultrasound – Useful when media is hazy; shows echogenic choroidal masses and associated retinal detachment.
- Magnetic Resonance Imaging (Brain + Orbit with Gadolinium) – Detects accompanying meningitis, optic-nerve sheath enhancement, or intra-ocular mass; T1-weighted images show ring-enhancing nodules.
Non-Pharmacological Treatments
Early and careful immune evaluation – identify and correct reversible immunosuppressive factors (e.g., tapering unneeded corticosteroids, reviewing immunosuppressive regimens). This reduces ongoing risk and improves response to antifungals. PMC
Prompt HIV testing and staging – in unknown status, testing for HIV and CD4 count allows targeted prevention and treatment (including timing of antiretroviral therapy). ClinicalInfo
Optimized antiretroviral therapy (ART) – for HIV-positive patients, getting on ART improves immune function long-term, but timing must balance the risk of IRIS. Coordination with cryptococcal therapy helps avoid harmful inflammatory surges. HIV GuidelinesMDPI
Monitoring and managing immune reconstitution inflammatory syndrome (IRIS) – surveillance and readiness to modulate inflammation if IRIS happens after ART initiation. This may include cautious use of anti-inflammatory therapy under specialist guidance. MDPINCBI
Frequent vision and ocular examinations – early detection of progression or complications allows timely intervention (e.g., biopsy or surgery). EyeWiki
Head-of-bed elevation and intracranial pressure (ICP) awareness – for patients with meningitis, managing raised ICP via serial lumbar punctures or other interventions reduces secondary ocular effects like papilledema. Oxford Academic
Diagnostic vitreous biopsy when unclear – used to confirm intraocular infection without waiting for systemic progression; that avoids delays in targeted therapy. PubMed
Avoidance of unnecessary corticosteroid use before antifungal coverage – indiscriminate steroids can worsen fungal spread; they are reserved for specific situations like IRIS or mass effect after antifungal therapy is established. PubMedBioMed Central
Education on environmental exposure – patients with high risk (e.g., advanced HIV) should be informed about common environmental sources (decaying wood, bird droppings) and practice cautious handling or avoidance in highly exposed settings. Medscape
Nutritional support – ensuring adequate calories, protein, and micronutrients (especially vitamin D, C, zinc, selenium) to support immune function, giving the body resources to cooperate with antifungal therapy. PMCPMC
Smoking cessation – smoking impairs mucosal immunity and systemic inflammation, potentially worsening outcomes in invasive infections. (Inference based on general immune impairment literature.) PMC
Good oral hygiene and infection control – minimizes additional infectious burdens which could further suppress immunity. General infection prevention principles.
Safe water and food handling – avoid secondary infections from contaminated sources while the immune system is working. ResearchGate
Supportive hydration and electrolyte management – especially when systemic illness causes fever or anorexia, maintaining physiologic state helps drug delivery and tolerance. (General medical best practice.)
Psychosocial support and adherence counseling – complex long treatment courses need sustained adherence; counseling improves outcomes. (Standard for chronic infections and HIV care.)
Regular neurologic and cognitive monitoring – concurrent meningitis can cause subtle neurologic decline; early detection avoids permanent damage. Oxford Academic
Avoidance of live vaccines during active infection – immune system is compromised; live vaccines may cause harm until recovery. (General immunocompromised patient guidance.)
Coordination with infectious disease and ophthalmology specialists – multidisciplinary care ensures appropriate sequencing of therapy and recognition of uncommon complications. Medscape
Use of protective eyewear in high-risk environments – while not specifically preventing bloodstream seeding, it reduces risk of superimposed ocular insults; general protective practice.
Monitoring for drug toxicity through labs and exam – consistent non-pharma oversight (e.g., kidney function with amphotericin) allows adjustment without pharmacologic missteps. World Health Organization
Drug Treatments
Note: Therapy usually follows three phases: induction (intensive), consolidation, and maintenance. Recommendations below reflect standards especially in HIV-associated cryptococcosis, which is the most common context for choroidal involvement. World Health OrganizationClinicalInfo
Liposomal Amphotericin B
Class: Polyene antifungal.
Dose: 3–4 mg/kg IV daily (as preferred by WHO/updated guidelines for induction in HIV-associated cryptococcal meningitis). High-dose single or short course strategies are also being used per recent WHO updates. World Health Organization
Timing: Induction phase, typically for 1–2 weeks depending on clearance and clinical response.
Side Effects: Nephrotoxicity (less than deoxycholate form), electrolyte abnormalities (hypokalemia, hypomagnesemia), infusion reactions, anemia. Monitoring kidney function is essential. World Health Organization
Amphotericin B deoxycholate
Class: Polyene antifungal.
Dose: 0.7–1.0 mg/kg IV daily (used if liposomal is not available).
Timing: Induction phase (longer toxicity profile).
Side Effects: Significant nephrotoxicity, infusion-related fevers/chills, electrolyte disturbances. Requires pre-hydration and close monitoring. World Health Organization
Flucytosine
Class: Pyrimidine analog antifungal.
Dose: 25 mg/kg orally four times daily (total 100 mg/kg/day), adjusted for renal function.
Timing: Used in combination with amphotericin B during induction (first 1–2 weeks); accelerates fungal clearance.
Side Effects: Bone marrow suppression (anemia, leukopenia), hepatotoxicity, gastrointestinal upset. Requires blood count monitoring. PMC
Fluconazole
Class: Azole antifungal.
Dose: Consolidation: 800 mg/day orally for 8 weeks, then maintenance 200 mg/day (or 3 mg/kg) for 6–12 months.
Timing: After successful initial induction; sometimes used alone if amphotericin is unavailable or for long-term prophylaxis/maintenance.
Side Effects: Hepatotoxicity (rare), QT prolongation (rare), drug interactions (CYP450). ClinicalInfo
Voriconazole (less common for cryptococcus but sometimes considered in eye involvement when standard therapy fails or for intolerance)
Class: Triazole antifungal.
Dose: 6 mg/kg IV every 12 hours for two doses then 4 mg/kg IV twice daily, or oral equivalent; dosage adjustments based on levels.
Timing: Salvage/alternative therapy in specific ocular or resistant cases.
Side Effects: Visual disturbances (blurred vision, photopsia), hepatotoxicity, skin photosensitivity, QT prolongation. (Note: Not first-line; used when standard agents are contraindicated or ineffective.)
Fluconazole High-Dose (800 mg) Alone
Class: Azole.
Use: In mild disease or when amphotericin and flucytosine are unavailable; less fungicidal so used for consolidation/maintenance.
Side Effects: As above; slower clearance so close monitoring required. Oxford Academic
Intravitreal Amphotericin B (for intraocular extension not controlled by systemic therapy)
Class: Local polyene antifungal injection.
Dose: Small-volume injections (e.g., 5–10 µg/0.1 mL) directly into vitreous at specialist discretion.
Purpose: Treat sight-threatening intraocular fungal lesions when systemic therapy alone fails. Often combined with vitrectomy. PubMedophthalmology.theclinics.com
Side Effects: Ocular toxicity if misdosed, inflammation, retinal damage if improperly administered.
Systemic Corticosteroids (selective, adjunctive use)
Class: Anti-inflammatory.
Use: Reserved for specific complications—like immune reconstitution inflammatory syndrome (IRIS), cryptococcomas with mass effect, or severe inflammatory swelling after fungal load has been reduced. Started cautiously after antifungal therapy is established; the evidence remains mixed and is situational. PubMedBioMed Central
Side Effects: Immunosuppression (if overused), hyperglycemia, mood changes, risk of worsening infection if used improperly.
Flucytosine with Fluconazole (alternative when amphotericin is contraindicated)
Use: In selected non-HIV or mild cases, combination may be used though less potent than amphotericin-based induction.
Side Effects: Sum of azole and flucytosine toxicities.
Adjunctive Interferon-gamma 1b
Class: Immunomodulator (cytokine).
Dose: Variable in trials (often 100 µg subcutaneously three times per week) added to standard antifungal therapy.
Purpose: Boosts macrophage and cellular antifungal response; has been shown in randomized trials to accelerate fungal clearance in cryptococcal meningitis, with potential extrapolation to severe disseminated disease including ocular involvement. PMCPubMedThe Lancet
Side Effects: Flu-like symptoms, fever, injection site reactions, potential autoimmunity activation.
Dietary Molecular Supplements
These are adjunctive—they do not replace antifungal therapy but support immune function, especially when deficiencies are present. Always check for interactions and avoid megadoses unless supervised.
Vitamin D3 (Cholecalciferol)
Dosage: 1000–2000 IU/day (adjust based on serum 25(OH)D levels).
Function: Modulates innate and adaptive immunity, enhances antimicrobial peptide production.
Mechanism: Vitamin D receptors on immune cells help regulate cytokine expression and promote macrophage function important in fungal defense. PMC
Vitamin C (Ascorbic Acid)
Zinc
Dosage: 15–30 mg elemental zinc/day (short course if deficient).
Function: Supports T-cell and macrophage function.
Mechanism: Cofactor in multiple enzymes, modulates cytokine production, stabilizes membranes against oxidative damage. ResearchGatePMC
Selenium
Dosage: 100 mcg/day (avoid excess).
Function: Antioxidant, modulates immune responses.
Mechanism: Component of glutathione peroxidases that protect immune cells and support regulation of inflammation. PMC
Omega-3 Fatty Acids (EPA/DHA)
Dosage: 1–2 grams/day of combined EPA/DHA.
Function: Regulate inflammation and support resolution.
Mechanism: Convert to specialized pro-resolving mediators, reducing harmful chronic inflammation while not suppressing necessary antifungal responses. PMC
Probiotics (e.g., Lactobacillus, Bifidobacterium)
Dosage: CFU counts in the billions daily, choose clinically studied strains.
Function: Maintain gut microbiome balance, indirectly supporting systemic immunity.
Mechanism: Gut-associated lymphoid tissue (GALT) influences systemic immune tone; a healthy microbiome can enhance resistance to opportunistic infections. MDPIResearchGate
Vitamin A (Beta-carotene precursors)
Dosage: Avoid high preformed vitamin A; use dietary sources or controlled supplementation (e.g., 5000 IU if deficient).
Function: Mucosal and epithelial barrier maintenance, lymphocyte function.
Mechanism: Supports differentiation of immune cells and integrity of mucosal surfaces. cnu.primo.exlibrisgroup.com
B-Complex Vitamins (Especially B6, B12, Folate)
Dosage: Standard daily multivitamin doses or specific supplementation if deficiency documented.
Function: Energy metabolism for immune cells, DNA synthesis in rapidly proliferating lymphocytes.
Mechanism: Cofactors in nucleotide synthesis and homocysteine metabolism, affecting immune cell proliferation. (General micronutrient immunology inference.)
N-acetylcysteine (NAC)
Dosage: 600–1200 mg/day.
Function: Antioxidant precursor to glutathione, reduces oxidative stress.
Mechanism: Replenishes intracellular glutathione to protect immune cells and tissues from damage during infection. (Supportive, extrapolated from general infection literature.)
Curcumin (from Turmeric)
Dosage: 500–1000 mg of bioavailable formulations/day.
Function: Mild immunomodulation and anti-inflammatory effect.
Mechanism: Inhibits NF-κB pathways and reduces excessive inflammation, which can assist balanced immune response without suppressing antifungal activity if used appropriately. (Adjunct; evidence in modulating infection-associated inflammation.)
Note: Always test for deficiencies before high-dose micronutrient therapy. Some (e.g., zinc, vitamin A) in excess can be harmful. PMCPMC
Immunomodulatory / “Regenerative” Therapies
Strictly speaking, classic “stem cell drugs” are not established for cryptococcal choroiditis. What has been explored to strengthen host immunity or modulate response includes:
Interferon-gamma 1b
Purpose/Mechanism: Enhances macrophage fungicidal activity and T-cell collaboration. Shown to speed clearance of Cryptococcus in meningitis when added to standard antifungal therapy. PMCPubMedThe Lancet
Dosage: Variable in trials (e.g., 100 µg subcutaneously three times weekly), usually as adjunct.
Status: Evidence-supported adjunct in research settings, especially for severe or refractory systemic disease.
Granulocyte-Macrophage Colony-Stimulating Factor (GM-CSF) (Investigational use)
Purpose/Mechanism: Stimulates differentiation and activation of macrophages and dendritic cells, potentially improving antigen presentation and fungal clearance.
Status: Limited data in cryptococcal disease; considered experimental or off-label, primarily in trials or specialist contexts. (Inference from broader immune-adjuvant literature; not standard-of-care.)
Interleukin-7 (IL-7) (Experimental)
Purpose/Mechanism: Supports T-cell survival and expansion, potentially restoring cellular immunity in lymphopenic states such as advanced HIV.
Status: Early clinical studies for immune reconstitution; not standard for cryptococcosis, and use would be in carefully controlled research settings.
Adoptive T-cell Therapy (Highly experimental)
Purpose/Mechanism: Infusing fungus-specific T cells to help immune control; conceptual for severe refractory infections.
Status: Preclinical/very early phase; not current standard, included to acknowledge regenerative immune concepts.
Mesenchymal Stem Cell (MSC) Paracrine Immunomodulation (Investigational, cautionary)
Purpose/Mechanism: MSCs can secrete factors that modulate immune inflammation; theoretical interest in modulating harmful inflammatory states like IRIS.
Status: No established role; data are preliminary, and uncontrolled use could be harmful. This is not a recommended treatment outside research.
Checkpoint Pathway Modulation (e.g., PD-1/PD-L1 inhibitors) (Theoretical/experimental)
Purpose/Mechanism: In some chronic infections, exhaustion of T cells via checkpoint pathways impairs clearance; modulation might restore function.
Status: Very early, with significant risks of triggering harmful inflammation—only in research with careful risk/benefit discussion.
Important: The last four are mostly investigational. They are included to clarify that while immune “regeneration” is a hopeful concept, the only reasonably evidence-backed adjunct currently for cryptococcal disease is interferon-gamma, and others remain experimental or theoretical. Avoid unregulated stem cell clinics. PMCPubMedThe Lancet
Surgical / Procedural Interventions
Diagnostic Vitreous Biopsy
Procedure: Surgical sampling of vitreous fluid through pars plana approach.
Why: To obtain direct evidence of fungal organisms when diagnosis is uncertain or ocular disease is not responding, guiding therapy. PubMed
Pars Plana Vitrectomy with Intravitreal Antifungal Injection
Procedure: Removal of infected vitreous (debulk fungal load) combined with direct injection of antifungal (e.g., amphotericin B) into the eye.
Why: For intraocular disease unresponsive to systemic therapy or with dense fungal masses (endophthalmitis component), this can arrest progression and salvage vision. PubMedophthalmology.theclinics.com
Management of Elevated Intracranial Pressure via Neurosurgical Shunting (e.g., Ventriculoperitoneal Shunt)
Procedure: Surgical diversion of CSF for refractory intracranial hypertension.
Why: Cryptococcal meningitis frequently elevates intracranial pressure; if serial lumbar punctures fail, shunting protects vision (by reducing optic nerve edema) and neurologic function. Oxford Academic
Surgery for Ocular Complications (e.g., Retinal Detachment Repair)
Procedure: Retinal reattachment procedures (e.g., scleral buckle, vitrectomy) when secondary structural damage (tractional or rhegmatogenous detachment) occurs after infection.
Why: Preserve or restore vision in the face of mechanical sequelae of inflammation/infection. (General ophthalmic complication management inference.)
Enucleation (Eye Removal)
Procedure: Surgical removal of the eyeball.
Why: Rarely used, reserved for severe, uncontrolled intraocular infection with pain and no visual potential, to prevent further systemic spread or relieve intractable discomfort. ophthalmology.theclinics.com
Key Prevention Strategies
Early HIV diagnosis and timely initiation of ART (with appropriate sequencing to avoid unmasking IRIS) – this reduces the incidence of cryptococcal disease by maintaining immune competence. ClinicalInfoHIV Guidelines
Screening for cryptococcal antigen in high-risk (CD4 <100) individuals before starting ART, to detect latent infection and treat early. World Health Organization
Primary prophylaxis with fluconazole in some high-risk settings (per local guidelines) when screening is not feasible or in persistently high-prevalence areas. World Health Organization
Avoid unnecessary chronic corticosteroid or immunosuppressive escalation without clear indication, particularly in persons with other risk factors. PMC
Environmental awareness: minimize exposure to bird droppings, decaying organic matter, and dusty environments in severely immunocompromised patients. Medscape
Maintain good nutrition to prevent micronutrient deficiencies that weaken immune responses. PMCPMC
Prompt treatment of other opportunistic infections that could further tax the immune system, preserving capacity to fight Cryptococcus. (General infectious disease principle.)
Adherence to antifungal prophylaxis or maintenance therapy when indicated, to prevent relapse in previously treated patients. PMC
Patient education about early warning signs so that vision changes or systemic symptoms prompt rapid medical evaluation.
Regular follow-up labs (e.g., CrAg titers in certain contexts) and imaging when indicated to catch recurrence early. Oxford Academic
When to See a Doctor
Seek immediate medical attention if any of the following occur:
New or worsening blurred vision or vision loss. EyeWiki
Floaters, flashes, or changes in visual fields.
Persistent headache, stiff neck, or neurological symptoms suggestive of meningitis. Oxford Academic
Fever or prolonged systemic illness in an immunocompromised person.
Eye pain or redness not explained by another cause.
Sudden changes after starting ART (possible IRIS). MDPI
Failure to improve on current antifungal therapy.
Signs of increased intracranial pressure (nausea, vomiting, vision changes). Oxford Academic
Any new ocular lesion noticed on self-exam or during routine ophthalmic check.
Recurrent symptoms after previous cryptococcal treatment indicating possible relapse. PMC
What to Eat and What to Avoid (Diet Guidance)
What to Eat (10 items):
Lean protein (eggs, poultry, legumes): supports immune cell production and repair.
Colorful fruits and vegetables (berries, citrus, leafy greens): rich in vitamins C, A precursors, and antioxidants. PMC
Fatty fish or omega-3 sources (salmon, flaxseed): modulate inflammation beneficially. PMC
Nuts and seeds (for selenium, zinc): supply trace minerals in bioavailable form. PMC
Whole grains (brown rice, oats): provide B vitamins and steady energy for immune function.
Yogurt or fermented foods with live cultures (if no contraindication): support gut-immune axis. ResearchGate
Vitamin D–rich foods (fortified milk, mushrooms exposed to UV): complement supplementation if levels are low. PMC
Hydrating fluids (clean water, broths): prevent dehydration that can worsen systemic illness.
Garlic and mild spices (in moderate amounts): some antimicrobial and immune-supportive properties, though not a replacement for therapy. (General supportive nutrition inference.)
Moderate citrus or papaya: natural vitamin C sources to aid cellular immunity. PMC
What to Avoid
Excessive sugar and ultra-processed foods: can blunt immune responsiveness.
Raw or undercooked meats and shellfish: risk of co-infection when immunity is low.
Unpasteurized dairy: potential source of other pathogens.
Excessive alcohol: suppresses immune function and interferes with medication metabolism.
High-dose self-prescribed supplements without testing (especially vitamin A, zinc) – risk of toxicity. PMC
Herbal remedies with unknown immunologic effects (some can suppress or unpredictably modify immunity).
Overcaffeinated drinks that cause poor sleep: sleep deficiency impairs immune recovery.
Foods that interact with antifungals (e.g., grapefruit with certain azoles) – check drug interactions if on voriconazole or fluconazole.
Unclean street food in severely immunocompromised states: avoid potential gastrointestinal infections.
Excessive iron supplementation unless deficiency proven: iron can, in theory, aid pathogen growth if unregulated. (General infection-nutrition consideration.)
Frequently Asked Questions (FAQs)
What causes cryptococcal choroiditis?
It is caused by spread of the fungus Cryptococcus neoformans (or less commonly C. gattii) into the eye, typically through the blood, in people with weak immune systems. EyeWikiWho is at risk?
People with advanced HIV/AIDS, transplant recipients, those on high-dose steroids or other immunosuppressants, and some cancer patients are highest risk. PMCClinicalInfoCan it happen if I have no symptoms in my eye?
Yes. Ocular lesions can exist with minimal inflammation, so systemic symptoms or routine eye exams may be how it’s first caught. EyeWikiHow is it diagnosed?
Diagnosis uses eye imaging (FA, ICG, OCT), blood and CSF cryptococcal antigen testing, CSF culture, and sometimes vitreous biopsy for direct sampling. EyeWikiPubMedIs it contagious to others?
No. The infection comes from environmental exposure and internal spread. It is not spread person-to-person via eye contact. (General infectious disease knowledge.)What is the main treatment?
Systemic antifungals—especially amphotericin B (often liposomal) with flucytosine initially, followed by fluconazole—are the backbone. Eye-directed therapy like intravitreal injections or surgery may be needed in progressive cases. World Health OrganizationClinicalInfoPubMedCan vision recover?
It depends on how early the infection is caught and how much structural damage occurred. Prompt, adequate treatment improves chances, but late or severe disease may leave permanent deficits. ophthalmology.theclinics.comDo I need surgery?
If the eye infection does not respond to drugs alone or if there is heavy vitreous involvement, vitrectomy with intravitreal antifungals or biopsy may be needed. In very extreme uncontrolled cases, enucleation could be considered. PubMedophthalmology.theclinics.comWhen should HIV treatment start if I have this infection?
ART is essential but should be timed to reduce risk of IRIS; generally, after initial antifungal induction and under specialist coordination, often within a few weeks based on clinical stability. HIV GuidelinesMDPICan dietary supplements cure it?
No. Supplements like vitamin D, C, zinc, and selenium only support immune health; they do not replace antifungal drugs. PMCPMCWhat is IRIS and how does it relate?
IRIS is an inflammatory syndrome that can occur when immune function rebounds (e.g., after starting ART), unmasking or worsening cryptococcal inflammation, including in the eye. Management may require careful anti-inflammatory therapy. MDPINCBIAre steroids ever used?
Yes, but only in limited situations (like cryptococcomas causing mass effect or IRIS) and only after antifungal burden is under control, because steroids can worsen fungal spread if misused. PubMedBioMed CentralHow long is treatment?
Induction is typically 1–2 weeks, consolidation about 8 weeks (high-dose fluconazole), and maintenance commonly for 6–12 months depending on immune recovery and underlying condition. PMCClinicalInfoCan it come back?
Yes. Relapse can occur, especially if maintenance therapy is stopped too early or immune suppression persists. Ongoing monitoring and adherence are critical. PMCIs there anything I can do to prevent it?
Maintain immune health (especially HIV control), screen high-risk individuals early, avoid high-risk exposures when severely immunocompromised, and take prophylactic antifungals in some settings as guided by clinicians. World Health OrganizationClinicalInfo
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Last Updated: August 01, 2025.
Crunch Syndrome
