Presumed Ocular Histoplasmosis Syndrome (POHS)

Presumed Ocular Histoplasmosis Syndrome (POHS) is an eye condition that leaves tiny “punched-out” scars in the retina and the layer under it (the choroid). Doctors spot a classic trio of signs: 1) small, round chorioretinal scars (often called “histo spots”), 2) thinning around the optic nerve head called peripapillary atrophy, and 3) trouble in the macula if new, fragile blood vessels grow there (choroidal neovascularization, or CNV). A key clue is what you don’t see: there is no inflammation floating in the eye’s gel (no vitritis). It’s called “presumed” because the fungus that likely triggered it years earlier is not found in the eye when you’re examined; we link it to past exposure by the pattern of the scars and where people have lived. EyeWikiBMJ Open

Many people are exposed to the soil fungus Histoplasma capsulatum, especially in parts of the central and eastern United States near the Ohio and Mississippi River valleys and in places with lots of bird or bat droppings. Most never have eye problems. In a small number, the immune system’s past reaction leaves tiny healed spots in the back of the eye. Years later, those quiet scars can set off abnormal vessel growth under the retina (CNV). These vessels leak, bleed, and scar, threatening sharp central vision used for reading and faces. The fungus itself is not active in the eye when POHS shows up, so antifungal pills are not a treatment for the eye disease; treatment focuses on stopping or preventing CNV. CDC+1ScienceDirect

Presumed Ocular Histoplasmosis Syndrome (POHS) is an eye condition that usually starts after a person breathes in tiny fungal spores called Histoplasma capsulatum. The body fights the germ in the lungs, and most people never feel sick. In some people, tiny spots of damage later show up in the back of the eye (the retina and choroid). Doctors look for three key signs: small “punched-out” scars in the retina (often called histo spots), a ring of thinning around the optic nerve called peripapillary atrophy (PPA), and no inflammation floating in the eye gel (no vitritis). Many people have no symptoms for years. Trouble starts when fragile, abnormal blood vessels grow under the retina (choroidal neovascularization, CNV), which can blur or distort central vision. These points come from large ophthalmology references. EyeWiki

The fungus lives in soil enriched with bird or bat droppings. It is common in the central and eastern United States—especially around the Ohio and Mississippi River Valleys—but it exists in many parts of the world. People are exposed by breathing dust from contaminated soil, caves, barns, or construction sites. CDC+2CDC+2

POHS means a person has old, healed marks in the back of the eye that strongly suggest a past Histoplasma exposure. These marks are the “histo spots” and the PPA ring. There is no active eye infection and no visible inflammatory cells floating in the eye. The disease is “silent” until abnormal blood vessels (CNV) grow through weak areas of the eye’s barrier layers (especially Bruch’s membrane) and leak or bleed under the central retina (the macula). When CNV forms, people notice blurred vision, crooked lines, or dark spots near the center of sight. EyeWikiPubMed

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Types

Doctors do not use a single official “staging chart” for POHS everywhere, but in everyday practice they often think about it in these simple buckets:

1. Inactive POHS (scars only).
   The eye shows histo spots and/or PPA. There is no CNV and no vitritis. People usually have no symptoms. This is often found during a routine eye exam. EyeWiki

2. POHS suspicious for new activity.
   The person still has old scars, but now reports new distortion or a gray spot. The doctor suspects early leakage or tiny new vessels starting under the macula and orders imaging to look for CNV. EyeWiki

3. POHS with active CNV.
   Abnormal blood vessels under the retina are present and leaking or bleeding. This is the form that threatens central vision and needs treatment. EyeWiki

4. POHS with disciform (healed) scar.
   The active CNV has burned out and left a thick scar under the macula. Vision loss here is usually permanent, and the goal becomes prevention in the other eye and monitoring for any new CNV. EyeWiki

5. Atypical or POHS-like presentations outside classic regions.
   Similar-looking scars can be seen in people who live far from U.S. endemic areas. Worldwide exposure is possible, so doctors consider travel, residence, and other causes of similar retinal scars. CDCPMC

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Causes

Important note: POHS has one main driver (past exposure to Histoplasma capsulatum). The other items below are best understood as risk factors, exposures, or mechanisms that increase the chances of getting POHS changes or of developing vision-threatening CNV later.

1. Past breathing in of Histoplasma spores (the root cause).
   People inhale spores from soil enriched with bird or bat droppings. The spores spread in the bloodstream and can reach the eye’s vascular layer (choroid), where tiny scars later form. EyeWikiCDC

2. Living in or long visits to endemic areas.
   The chance of exposure is much higher in the Ohio–Mississippi River Valley region of the U.S., where many adults test positive for past exposure. CDC+1

3. Soil-disturbing activities.
   Farming, excavation, bulldozing, and construction can kick spores into the air. CDC

4. Cave exploration (“spelunking”).
   Caves often contain bat droppings, which can carry the fungus. Breathing dust during caving increases exposure. EyeWiki

5. Bird or bat roost exposure (barns, attics, bridges).
   Cleaning old chicken coops, barns, or attics can aerosolize spores. CDC

6. Rural residence (population-level risk).
   Modern studies show people in rural areas have higher odds of POHS, even after considering other factors. PMC

7. Smoking (risk for CNV once POHS scars exist).
   Smoking roughly triples the chance of developing CNV in eyes with POHS scars, which is the step that harms central vision. EyeWikiPubMedScienceDirect

8. Older age (risk for CNV).
   With age, eye tissues like Bruch’s membrane become more fragile, making it easier for abnormal vessels to break through at old scar edges. EyeWiki

9. Lower educational level (a proxy exposure signal).
   Some research links lower educational level with higher CNV risk in POHS, possibly due to more smoke exposure or environmental work; the biology is not direct but the association is observed. EyeWiki

10. Genetic immune markers (HLA) that may raise susceptibility.
    HLA-DRw2 and HLA-B7 show higher rates in people with certain POHS scar patterns, suggesting a genetic tendency in how the immune system responds. EyeWiki

11. Prior lung infection with Histoplasma.
    The lung is the first stop. From there, the organism (or the immune reaction to it) can affect the choroid and leave scars behind. Cleveland Clinic

12. Inflammatory healing that leaves weak spots.
    The body’s repair process can produce small breaks in Bruch’s membrane. Later, CNV can sprout through these weak points. PubMed

13. Heavy lifetime exposure during childhood in endemic areas.
    A very high share of adults in the “Histo Belt” show evidence of past exposure, meaning many are primed for the retinal scar pattern even if they never felt sick. CDC

14. Occupations with frequent dusty soil contact (farm, demolition, construction, bridge/steel work).
    Regular, unprotected work in contaminated environments raises exposure chances. CDC

15. Bat- or bird-infested building cleanup without protection.
    Not wearing proper masks and not wetting down dust increases spore inhalation risk. CDC

16. Worldwide travel or residence in other endemic zones.
    Histoplasma also lives in parts of Central/South America, Africa, Asia, and Australia; exposure can happen outside the U.S. CDC

17. Possible contribution from diabetes (being studied).
    Observational work has explored diabetes as a risk factor for POHS; this remains a research signal rather than a proven cause. Johns Hopkins University

18. Secondhand smoke exposure (population signal).
    Studies proposing links between lower education and CNV in POHS suggest more smoke exposure may be involved, though this is an indirect association. EyeWiki

19. The body’s own growth signals (VEGF) at scar edges.
    Scar-related stress and hypoxia can drive VEGF release, encouraging CNV to grow through the old lesions. This is why anti-VEGF shots help when CNV appears. EyeWiki

20. Histoplasmin skin testing (historical note) may aggravate the eye.
    Old reports warn that skin testing for histoplasmosis can worsen POHS; it is not routinely recommended for classic cases. PMCEyeWiki

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Symptoms

1. Blurry central vision.
   The center of sight looks out of focus, especially for reading or faces. This often means CNV is active. EyeWiki

2. Wavy or crooked lines (metamorphopsia).
   Straight lines on a page or tile floor look bent.

3. A gray or dark spot near the center (scotoma).
   A small patch blocks part of letters or faces.

4. Sudden drop in reading vision.
   Words fade, jumble, or skip.

5. Colors look washed out.
   Reds or blues feel dull compared with the other eye.

6. Poor contrast.
   Pale text on a gray background is hard to see.

7. Need for more light to read.
   Bright light helps but does not fix the blur.

8. Trouble with fine detail.
   Sewing, small fonts, or phone icons get difficult.

9. Distorted shapes.
   Squares look like trapezoids; circles look oval.

10. Slow recovery after bright light (photostress).
    The “after-image” lingers longer than it used to.

11. Blind spots just off center.
    A small hole or smudge blocks part of a word.

12. New floaters are not typical in POHS.
    POHS lacks vitritis; new floaters suggest another problem and deserve a check. EyeWiki

13. Painless change.
    CNV changes vision without eye pain. EyeWiki

14. Symptoms often start in one eye.
    The other eye may be fine or only have old scars. EyeWiki

15. Sometimes no symptoms at all.
    Many people discover POHS scars during routine exams; symptoms begin only when CNV forms. EyeWiki

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Diagnostic tests

A) Physical exam (doctor-performed in the clinic)

1. Visual acuity (distance and near) with pinhole.
   Checks how clearly you see. Pinhole helps separate blur from refractive error. Sudden central blur suggests macular trouble from CNV.

2. Pupil exam for a relative afferent pupillary defect (RAPD).
   Looks for asymmetric optic nerve or macular function. Usually normal in small, unilateral lesions.

3. Confrontation visual fields.
   Rapid check for scotomas. A central or paracentral gap can align with a macular CNV.

4. Color vision testing.
   Macular disease can wash out red-green or blue-yellow contrast.

5. Contrast sensitivity.
   Finds subtle macular loss even when letter charts look “okay.”

6. Slit-lamp and dilated fundus exam.
   The key bedside test. Doctors look for no vitritis, look carefully for histo spots, a PPA ring, and any signs of active CNV (subretinal fluid, hemorrhage). EyeWiki

B) “Manual” vision tests (office or home tools you use)

7. Amsler grid.
   A simple grid of squares to check for new wavy lines or missing boxes at home or in the clinic. It helps catch early CNV. EyeWiki

8. Photostress recovery test.
   A bright light briefly bleaches the macula; slow recovery hints at macular pathology.

9. Brightness acuity (glare) testing.
   Looks for macular sensitivity issues masked by normal room lighting.

10. Goldmann manual kinetic perimetry.
    A detailed, technician-guided map of visual fields that can show central or paracentral defects from macular lesions.

C) Laboratory and pathological tests (to assess exposure or rule out other disease)

11. Histoplasma urine antigen (EIA).
    Helpful for active systemic histoplasmosis; not required for classic POHS but used if systemic disease is suspected. CDC

12. Serologic antibody tests (complement fixation, immunodiffusion).
    Can show prior exposure, but many POHS patients test negative. Results do not change eye management when the fundus picture is classic. EyeWiki

13. Fungal culture or tissue pathology (outside the eye).
    Used only when systemic infection is being worked up; not part of routine POHS evaluation. CDC

14. General blood work to exclude mimics.
    Doctors may order tests (e.g., inflammatory or infectious panels) if the scars look atypical and they want to rule out other causes of chorioretinal scars.

Why skin testing isn’t used now: Histoplasmin skin tests are not routine for classic POHS and have been reported to exacerbate the condition; so clinicians avoid them. PMC

D) Electrodiagnostic tests (how the retina and pathway are functioning)

15. Full-field electroretinogram (ERG).
    Tests the whole retina’s electrical response; in POHS it is often near normal unless disease is widespread.

16. Multifocal ERG.
    Samples many small retinal areas at once; can show reduced macular function around histo spots or CNV.

17. Visual evoked potentials (VEP).
    Checks the signal along the optic nerve to the brain; used if the doctor wants to separate macular from optic nerve problems.

E) Imaging tests (the most decisive tools for CNV)

18. Optical coherence tomography (OCT).
    A fast, painless “retinal ultrasound with light.” It shows fluid, pigment epithelial detachment, or scar tissue under the macula and helps monitor treatment. In POHS, histo spots line up with outer retinal atrophy on OCT. EyeWiki

19. Fluorescein angiography (FA).
    A dye test that shows leaking CNV and “window defect” hyperfluorescence over atrophic scars or PPA. It helps confirm activity and plan treatment. EyeWiki

20. OCT angiography (OCT-A) ± indocyanine green angiography (ICG).
    OCT-A shows the abnormal vessel network without dye and can detect subtle CNV when OCT or FA look stable; ICG helps reveal occult CNV and choroidal changes. EyeWiki

Non-pharmacological treatments

1. Education about warning signs – Purpose: catch CNV early. Mechanism: knowing to seek care for new distortion or a central blind spot leads to faster treatment and better outcomes.

2. Amsler grid self-monitoring (daily) – Purpose: home detection of wavy lines or missing squares. Mechanism: early CNV shifts the grid; you call your retina clinic right away.

3. Scheduled retina follow-ups – Purpose: surveillance of quiet histo spots. Mechanism: OCT/clinical checks catch silent fluid before vision drops.

4. Smoking cessation – Purpose: lower your risk of CNV and treatment burden. Mechanism: smoking worsens choroidal circulation and VEGF-driven changes; quitting reduces these stresses.

5. High-quality UV-blocking sunglasses and a brimmed hat – Purpose: reduce photochemical stress on the macula. Mechanism: filters high-energy light that can aggravate retinal oxidative stress.

6. Task lighting and contrast hacks – Purpose: make reading easier if vision is reduced. Mechanism: more light and higher contrast enlarge the “signal” your macula receives.

7. Magnification (handheld, stand magnifiers, digital zoom) – Purpose: boost readability. Mechanism: larger letters recruit more healthy retina around damaged spots.

8. Electronic aids (e-readers, text-to-speech, screen magnifiers) – Purpose: maintain independence. Mechanism: software enlarges and clarifies text; TTS bypasses visual demand.

9. Low-vision rehabilitation – Purpose: train practical work-arounds. Mechanism: therapists teach scanning, eccentric viewing, and device use tailored to your tasks.

10. Driving safety evaluation – Purpose: keep you and others safe. Mechanism: formal assessments and state rules match vision to driving demands; alternatives discussed if needed.

11. Workplace and school accommodations – Purpose: preserve productivity. Mechanism: large-print materials, high-contrast themes, adjustable monitors, and flexible seating.

12. Fall-prevention at home – Purpose: reduce injury when depth perception is off. Mechanism: decluttering, non-slip mats, and night-lights limit trip hazards.

13. Heart-healthy exercise (approved by your clinician) – Purpose: support retinal and choroidal blood flow. Mechanism: exercise improves vascular function and reduces systemic inflammation.

14. Blood pressure, glucose, and lipid control – Purpose: protect the micro-circulation that feeds the macula. Mechanism: stable cardio-metabolic numbers reduce endothelial stress.

15. Stress and sleep management – Purpose: steady hormones and inflammation that can worsen vascular leakage. Mechanism: better sleep lowers sympathetic surges and oxidative stress.

16. Safe work practices in endemic areas – Purpose: avoid heavy Histoplasma exposure (good general health practice even though it doesn’t “treat” POHS). Mechanism: N95 respirators, wetting soil, and avoiding bat/bird-dropping dust reduce inhalation of spores. CDC

17. Limiting second-hand smoke – Purpose: further lower CNV risk. Mechanism: removes smoke-related oxidative and vascular stressors.

18. Healthy body weight and anti-inflammatory diet pattern – Purpose: support retinal health. Mechanism: more antioxidants and omega-3s, fewer ultra-processed foods.

19. Medication adherence and appointment reminders – Purpose: keep injections and checks on time. Mechanism: consistent VEGF suppression prevents rebound leakage.

20. Vaccination and infection prevention (general health) – Purpose: protect overall wellness during treatment. Mechanism: staying healthy helps you attend visits and recover from procedures.

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Drug treatments

Important: Drug details here are general. Your retina specialist personalizes the agent and schedule.

1. Ranibizumab 0.5 mg intravitreal injection
   Class: anti-VEGF monoclonal antibody fragment. Schedule: Often monthly at first, then “treat-and-extend” as the eye dries on OCT. Purpose: Stop/leeching CNV activity and preserve or improve center vision. Mechanism: Blocks VEGF-A, the main growth factor driving abnormal vessels. Side effects: transient eye irritation, tiny floaters; rare serious events include endophthalmitis or retinal tear/detachment. Strong real-world and extrapolated evidence supports anti-VEGF for CNV in POHS. PubMedAAO

2. Bevacizumab 1.25 mg intravitreal (off-label for eye)
   Class: anti-VEGF monoclonal antibody. Schedule: about every 4–6 weeks initially, then extend if stable. Purpose/Mechanism: same VEGF-A blockade; widely used for cost and effectiveness. Side effects: similar ocular risks to other injections; systemic risks appear low at eye doses. (Commonly used off-label for CNV, including POHS.) PubMed

3. Aflibercept 2 mg intravitreal
   Class: VEGF-trap fusion protein. Schedule: Often monthly for 3 doses, then every 8 weeks or treat-and-extend based on OCT. Purpose: Dry the macula and suppress CNV. Mechanism: Binds VEGF-A, VEGF-B, and PlGF with high affinity. Side effects: as above; generally well tolerated. (Extrapolated from neovascular AMD/secondary CNV literature and clinical practice in POHS.) AAO

4. Faricimab 6 mg intravitreal
   Class: bispecific antibody to VEGF-A and Ang-2. Schedule: Often every 4–8 weeks then extended if stable. Purpose/Mechanism: Dual pathway control (VEGF + vascular stabilization via Ang-2). Side effects: similar injection risks; faricimab has an expanding safety record in other CNV diseases; used by some clinicians for difficult POHS CNV. (Evidence base emerging; off-label in POHS.)

5. Brolucizumab 6 mg intravitreal
   Class: small single-chain antibody fragment to VEGF-A. Schedule: loading then possible 12-week intervals if safe. Purpose: potent drying in tough CNV. Mechanism: dense molar dosing of anti-VEGF. Side effects: rare but serious retinal vasculitis/occlusive events; careful risk-benefit discussions are essential.

6. Verteporfin (Visudyne) photodynamic therapy (PDT)
   Class: photosensitizer drug + cold laser. Dose/Timing: infused intravenously at 6 mg/m² over 10 min; a non-heating laser is applied to the CNV spot 15 min after infusion; sessions can be repeated if leakage persists. Purpose: selectively close CNV while sparing overlying retina. Mechanism: drug accumulates in abnormal vessels; laser activates it to generate reactive oxygen species that seal leaky vessels. Side effects: light sensitivity for several days, infusion-site pain, rare back pain; avoids thermal scarring of classic laser. PDT is an accepted option for CNV due to AMD, myopia, and POHS. AetnaPMC

7. Intravitreal triamcinolone acetonide (adjunct in select cases)
   Class: corticosteroid. Dose: commonly 2–4 mg intravitreal. Purpose: reduce leakage and inflammation around CNV resistant to anti-VEGF alone. Mechanism: down-regulates inflammatory cytokines and permeability. Side effects: cataract acceleration, intraocular pressure rise, infection risk. Some studies suggest steroid + anti-VEGF can help in POHS CNV, but practice varies. PMC+1

8. Dexamethasone intravitreal implant (0.7 mg, Ozurdex®) — adjunct
   Class: biodegradable steroid implant. Timing: releases drug over ~3 months. Purpose/Mechanism: similar to triamcinolone with a slow-release profile. Side effects: pressure spikes and cataract risk; used selectively for refractory leakage.

9. Topical/Oral antifungals — not indicated for POHS
   Class: antifungal agents. Purpose: none for inactive POHS. Mechanism: they target live fungus, but POHS eye disease is not an active fungal infection. Side effects: unnecessary risk if used without indication. ScienceDirect

10. Peri-lesional or sub-Tenon steroid (selective)
    Class: corticosteroid injection near the eye wall. Purpose: very selected adjunct in inflammatory overlap cases judged by a retina/uveitis specialist. Mechanism/Side effects: steroid effects as above; not routine for classic, non-inflamed POHS.

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Dietary “molecular” supplements

Note: No supplement has proven to prevent or cure POHS. These aim to support retinal health generally. Discuss with your clinician, especially if pregnant, on blood thinners, or with kidney/liver disease.

1. Lutein 10 mg + Zeaxanthin 2 mg daily – pigments that concentrate in the macula and may bolster antioxidant defenses.

2. Omega-3 fatty acids (EPA+DHA 1,000–2,000 mg/day) – support retinal cell membranes and may dampen inflammatory signaling.

3. Vitamin C (500 mg/day) – water-soluble antioxidant supporting collagen and vessel integrity.

4. Vitamin E (≤200 IU/day unless otherwise advised) – lipid-phase antioxidant; avoid high doses if on anticoagulants.

5. Zinc (10–25 mg elemental/day) – cofactor for retinal enzymes; high doses can upset stomach/copper; don’t exceed advised limits.

6. Copper (1–2 mg/day if taking zinc) – prevents copper deficiency anemia when zinc intake is higher.

7. Astaxanthin (6–12 mg/day) – carotenoid with strong antioxidant capacity; early visual-fatigue data exist, not POHS-specific.

8. Alpha-lipoic acid (200–600 mg/day) – recycles other antioxidants; caution with hypoglycemia in diabetics.

9. Resveratrol (100–250 mg/day) – polyphenol with vasoprotective signaling in preclinical studies.

10. Bilberry/anthocyanins (80–160 mg/day standardized) – plant flavonoids with antioxidant/vascular effects.

These are supportive only; anti-VEGF/PDT decisions still drive outcomes.

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Regenerative / stem-cell drugs

There are no approved immune-boosting, regenerative, or stem-cell drugs for POHS. Unregulated stem-cell eye injections have caused blindness in other retinal diseases. For POHS, the proven path is anti-VEGF therapy, sometimes combined with PDT, plus careful monitoring. If you’re curious about research options, ask your retina specialist about clinical trials; trial therapies are monitored for safety and evidence. Until then, steer clear of “stem-cell” or “immunity booster” claims for POHS. AAO

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Procedures/surgeries

1. Intravitreal anti-VEGF injections – Technically a procedure. A tiny needle delivers medicine inside the eye in seconds. Why: first-line treatment to shut down CNV activity and save central vision. AAO

2. Photodynamic therapy (PDT) with verteporfin – An IV drug plus a cool laser targets the CNV selectively. Why: as an alternative or add-on when anti-VEGF alone is insufficient or to reduce injection burden. Aetna

3. Thermal laser photocoagulation (select extrafoveal lesions) – A focused heat laser seals leaky vessels only when they are far enough from the fovea to avoid central vision damage. Why: can permanently close well-placed CNV but risks scotoma and scar expansion.

4. Submacular surgery (historic/rare now) – Removing CNV membranes under the macula. Why: largely abandoned because outcomes were worse and complications higher than modern anti-VEGF care. EyeWiki

5. Pneumatic displacement ± tPA for large submacular hemorrhage – A gas bubble (and sometimes clot-dissolving medicine) repositions blood away from the fovea, usually followed by anti-VEGF. Why: give the macula a better chance when bleeding is heavy (not POHS-specific). EyeWiki

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Prevention tips

1. Know your risk if you lived or worked in endemic regions; get baseline retina exams. CDC

2. Don’t smoke; quit if you do. This lowers the risk of CNV in POHS.

3. Use an Amsler grid weekly and call promptly for new distortion.

4. Keep scheduled checkups even when vision “feels fine.”

5. Protect eyes from intense sunlight with UV-blocking lenses and hats.

6. Control blood pressure, lipids, and blood sugar.

7. Exercise regularly as cleared by your clinician.

8. Practice safe soil/dust handling in barns, attics, caves, or demolition: wet surfaces, wear an N95, and avoid stirring droppings. CDC

9. Eat a produce-rich, minimally processed diet that supports vascular health.

10. Use medications as prescribed and don’t miss injection visits—consistency matters for CNV control.

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When to see a doctor

• New wavy or bent lines, missing spots, or a gray/black patch in central vision

• Sudden drop in reading or face recognition

• Any new bleeding or floaters after treatment

• Persistent eye pain, pus, or vision loss after an injection or laser

• You have POHS and are pregnant or planning pregnancy—just to align follow-ups

• You lived in endemic areas and notice any central-vision symptoms

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What to eat and what to avoid

Eat more of:

1. Leafy greens (spinach, kale) for lutein/zeaxanthin.

2. Bright vegetables and berries (peppers, carrots, blueberries) for antioxidants.

3. Fatty fish (2–3×/week) for omega-3s.

4. Nuts and seeds (almonds, walnuts, flax) for healthy fats and minerals.

5. Citrus and tomatoes for vitamin C and carotenoids.

Limit/avoid:

1. Smoking and second-hand smoke (biggest avoidable risk).
2. Ultra-processed snacks and trans-fats that drive inflammation.
3. Sugary drinks that spike glucose and oxidative stress.
4. Excess alcohol which impairs nutrient absorption and healing.
5. Extreme salt if you have hypertension (protects micro-vasculature).

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Frequently Asked Questions

1. Is POHS an active fungal eye infection?
   No. It reflects old exposure; the eye disease now is not an active infection, and antifungal pills don’t help for the eye. ScienceDirect

2. What actually threatens my vision?
   Choroidal neovascularization (CNV) in or near the macula. The fragile vessels leak/bleed, blurring central sight.

3. What’s the main treatment if I get CNV?
   Intravitreal anti-VEGF injections. They are the proven first-line therapy and often stabilize or improve vision. AAO

4. How many injections will I need?
   It varies. Many people start monthly, then the interval is slowly extended if OCT shows the macula is dry. Your eye’s response sets the schedule.

5. Is bevacizumab safe if it’s off-label?
   It’s widely used off-label for eye diseases with strong clinical experience supporting effectiveness and safety at eye doses. Discuss pros/cons and alternatives with your specialist. PubMed

6. When is photodynamic therapy used?
   PDT with verteporfin is considered when anti-VEGF alone isn’t enough or to reduce injection frequency in select CNV patterns. Aetna

7. Do I ever need “regular” hot laser?
   Sometimes, if the CNV is well outside the center (extrafoveal). It’s avoided near the fovea because it can scar central vision.

8. Are big surgeries still done for POHS CNV?
   Old operations like submacular surgery or macular translocation have largely been abandoned because modern injections work better and are safer. EyeWiki

9. Can vitamins cure POHS?
   No. A healthy diet and reasonable supplements support eye health, but they don’t replace anti-VEGF or PDT when CNV appears.

10. Should I take antifungals just in case?
    No; they do not treat POHS eye disease and can cause side effects if taken without a medical need. ScienceDirect

11. Is POHS contagious?
    No. You can’t catch it from another person.

12. I lived in the “Histo Belt.” Do I automatically get POHS?
    No. Many people are exposed; only a small fraction develop the eye changes that define POHS. CDCPMC

13. What if I’m pregnant or planning to be?
    Tell your retina doctor. Timing of visits and the choice of medicines are coordinated carefully in pregnancy.

14. Can I exercise?
    Yes—heart-healthy activity is encouraged unless your doctor advises otherwise. Protect your eyes and stay consistent with injections.

15. How will I know if CNV comes back?
    Use the Amsler grid weekly and keep your appointments. Call immediately for new distortion or a central blind spot.

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

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

Last Updated: August 22, 2025.