Malarial Retinopathy

Malarial retinopathy means changes in the back of the eye (the retina) that happen during severe malaria, most often with Plasmodium falciparum. The retina is the light‑sensing layer that sends pictures to the brain. In severe malaria, sticky infected red blood cells block tiny blood vessels in the retina. This causes parts of the retina to lose oxygen, leak, and bleed. Doctors can see these changes with a special light (an ophthalmoscope) after putting safe dilating drops in the eye.

Malarial retinopathy is the eye (retina) involvement seen in people—especially children—with severe or cerebral malaria (usually from Plasmodium falciparum). The parasite makes infected red blood cells sticky. These cells clog tiny retinal vessels, causing patches of retinal whitening, white-centered hemorrhages, color changes in blood vessels (they can look orange/white), and sometimes swollen optic discs (papilledema). Doctors can see these signs by looking inside the eye with a dilated fundus exam. These eye changes mirror what’s happening in the brain’s small vessels—so the retina becomes a “window” to the brain in severe malaria. PMC+1Aetna

Why it matters: these eye signs are strong clues that the patient has cerebral malaria, not another cause of coma or severe illness. The eye can act like a “window” to what is happening in the brain’s small vessels. When present, malarial retinopathy helps doctors confirm the diagnosis, judge how severe the disease is, and follow recovery.

Common eye signs include:

  • Retinal whitening: pale patches in the retina where blood flow is low.
  • Retinal hemorrhages: small bleeds, often with a pale center.
  • Abnormal vessel color: orange‑white streaks instead of the normal red.
  • Swollen optic disc (papilledema): the “entry point” of the optic nerve looks raised, showing pressure in the head.

In children, these signs are very helpful to confirm cerebral malaria. In adults, the signs can also appear but are often milder. Many patients are too sick or drowsy to report eye symptoms, so careful eye examination is key.


Types

Doctors use several simple ways to group malarial retinopathy. These “types” help describe what is seen, how serious it is, and who is affected.

  1. By dominant feature
  • Ischemic‑dominant type (whitening‑predominant): pale patches from low blood flow are the main sign.
  • Hemorrhagic‑dominant type: many small bleeds (some with pale centers) are the main sign.
  • Mixed type: both pale patches and bleeds are common.
  1. By vessel change
  • With vessel color change: arteries and veins look orange‑white instead of red, a very specific sign for severe malaria.
  • Without vessel color change: other retinal signs are present but vessel color looks normal.
  1. By location in the retina
  • Macula‑predominant: changes cluster in the macula (the sharp‑vision area), often linked with reduced central vision.
  • Peripheral‑predominant: changes mostly in the outer retina; may be missed without widefield viewing.
  1. By severity
  • Mild: a few small pale patches or bleeds; no swelling of the optic disc.
  • Moderate: multiple pale patches and bleeds; may have mild disc swelling.
  • Severe: large areas of whitening, many bleeds, marked vessel color change, and clear disc swelling.
  1. By patient group
  • Pediatric type: common in children with cerebral malaria; signs are usually obvious.
  • Adult type: can occur in adults; signs may be fewer or subtler.
  1. By time course
  • Acute: seen during the severe illness.
  • Resolving: signs shrinking over days to weeks after treatment.
  • Resolved: eye looks normal again; this is common after recovery.

 Causes

Think of each cause below as a factor that produces or worsens the retinal changes during severe malaria.

  1. Infection with Plasmodium falciparum: this parasite is the main trigger. It invades red blood cells and makes them sticky.
  2. Cytoadherence (stickiness) of infected red cells: the parasite puts proteins on the red cell surface that make the cell cling to the vessel wall, blocking flow.
  3. Rosetting and clumping: infected cells stick to normal red cells and to each other, making thick clumps that clog tiny vessels.
  4. Micro‑vessel blockage and low oxygen (ischemia): blocked capillaries starve the inner retina of oxygen, causing whitening and vision loss.
  5. Endothelial activation: the vessel lining becomes inflamed and “activated,” making it even easier for sticky cells to attach and for fluid to leak.
  6. Blood–retina barrier leak: the normal seal between blood and retina breaks down, letting plasma leak out, which causes swelling and pale patches.
  7. Thrombocytopenia (low platelets): fewer platelets mean the retina bleeds more easily, so small hemorrhages appear.
  8. Coagulation changes: malaria can tip the balance toward clotting in small vessels (microthrombi), adding to blockage and tiny bleeds.
  9. Severe anemia: too few red cells means poor oxygen delivery, worsening retinal hypoxia and whitening.
  10. Metabolic acidosis (high blood acid / raised lactate): low pH and high lactate reflect poor tissue oxygen; this goes with more severe retinal damage.
  11. Hypoglycemia (low blood sugar): harms retinal and brain cells, especially in children; may add to visual dysfunction.
  12. High parasite biomass: a heavy parasite load means more sticky cells to clog vessels and more severe eye signs.
  13. Inflammatory cytokines (e.g., TNF‑α, IFN‑γ): chemical messengers rise in severe malaria, driving endothelial damage and leak.
  14. Low nitric oxide (NO) bioavailability: less NO means tighter, less flexible vessels and poorer blood flow.
  15. Raised intracranial pressure (papilledema): swelling pressure from the brain pushes on the optic nerve head, making it look swollen.
  16. Dehydration and hemoconcentration: thicker blood flows more slowly in tiny vessels, promoting blockages.
  17. Bacterial co‑infection or sepsis: can worsen inflammation and clotting problems, adding to retinal bleeding and ischemia.
  18. Delayed or inadequate antimalarial therapy: allows ongoing sequestration and microvascular injury in the retina.
  19. Parasite surface protein variants (PfEMP1/var genes): some variants prefer brain and retinal vessels, increasing risk of eye signs.
  20. Vitamin A deficiency (association): low vitamin A has been linked with worse retinopathy in some studies, possibly through weaker barrier function.

Symptoms

Many patients with severe malaria are drowsy or in coma, so they cannot describe eye symptoms. When patients are awake enough to report, these are common complaints. Caregivers and clinicians should also watch for the signs listed.

  1. Blurred vision: things look out of focus, especially for reading or seeing faces.
  2. Central blind spot or hazy center: trouble seeing fine details in the middle of vision (central scotoma).
  3. Patchy missing areas: parts of the scene seem missing or dim (paracentral scotomas).
  4. Poor color vision: colors, especially red, look washed out.
  5. Sensitivity to light (photophobia): bright light is uncomfortable.
  6. Poor night vision: harder to see in dim rooms.
  7. Seeing dark spots or floaters: tiny moving specks from small bleeds.
  8. Headache: common in malaria and with raised pressure in the head.
  9. Fever with chills and sweats: classic malaria symptoms; eye signs often appear during severe fever.
  10. Drowsiness or confusion: warning signs of cerebral malaria.
  11. Seizures: may occur in severe malaria and point to brain involvement.
  12. Nausea and vomiting: common in severe illness and high fever.
  13. Severe tiredness or weakness: due to anemia and infection.
  14. Fast breathing: can signal acidosis or lung involvement.
  15. Eye discomfort or pressure: sometimes reported if the optic disc is swollen.

Important: Some patients have no eye symptoms, and the only clues are the findings on eye examination. That is why a careful dilated fundus exam is so valuable in severe malaria.


Diagnostic Tests

Below are the key tests used to diagnose malarial retinopathy and its cause (severe malaria). The numbers add up to 20 tests in five groups. Each entry explains what the test is and why it helps.

A) Physical Examination

  1. General exam and vital signs: temperature, pulse, blood pressure, breathing rate, and oxygen saturation. Purpose: confirm severe infection and shock. Mechanism: shows how the whole body is coping with malaria.
  2. Neurologic exam with coma scale (Blantyre or Glasgow): checks alertness, behavior, and motor responses. Purpose: detect cerebral malaria. Mechanism: brain dysfunction often accompanies retinal signs.
  3. External eye and pupil light reflex check: looks at eye alignment, eyelids, conjunctival pallor (anemia), scleral icterus (jaundice), and if pupils react to light. Purpose: screen for anemia, liver stress, and optic nerve function. Mechanism: severe disease affects multiple systems.
  4. Dilated fundus exam at bedside (direct or indirect ophthalmoscopy): the core test. Purpose: directly see retinal whitening, hemorrhages (often with pale centers), vessel color changes, and papilledema. Mechanism: reveals microvascular blockage and leak in real time.

B) Manual (Bedside) Vision Tests

  1. Visual acuity test (near or distance chart): measures clarity of vision. Purpose: gauge impact on daily seeing. Mechanism: macular involvement lowers acuity.
  2. Confrontation visual fields: simple bedside mapping of missing areas. Purpose: detect central or paracentral scotomas. Mechanism: retinal ischemia creates patchy field loss.
  3. Color vision or red‑desaturation test: quick check of color sharpness. Purpose: pick up macular or optic pathway stress. Mechanism: ischemia reduces color sensitivity.
  4. Amsler grid: handheld grid for central vision. Purpose: reveals wavy lines or missing boxes in macula disease. Mechanism: macular whitening distorts grid perception.

C) Laboratory and Pathological Tests

  1. Thick and thin blood smear microscopy: gold standard to identify malaria species and count parasites. Purpose: confirm malaria and measure load. Mechanism: shows infected red cells.
  2. Rapid diagnostic tests (HRP2 and/or pLDH antigens): quick finger‑prick tests. Purpose: support diagnosis when microscopy is delayed. Mechanism: detect parasite proteins.
  3. Complete blood count (CBC): checks hemoglobin (anemia) and platelets (often low). Purpose: explain pallor, bleeding risk. Mechanism: severe malaria commonly causes anemia and thrombocytopenia.
  4. Serum glucose: spot low blood sugar. Purpose: urgent correction to protect brain and retina. Mechanism: hypoglycemia harms neurons.
  5. Serum lactate and blood gas (acid–base): measure tissue oxygen debt and acidosis. Purpose: grade severity and risk. Mechanism: high lactate matches worse retinal and brain ischemia.
  6. Coagulation profile (PT/INR, aPTT, D‑dimer): screens for clotting trouble. Purpose: explain widespread small bleeds. Mechanism: malaria can trigger microthrombi and bleeding.

D) Electrodiagnostic Tests

  1. Electroretinography (ERG): records the retina’s electrical response to light. Purpose: assess how well retinal cells work during and after illness. Mechanism: ischemia can reduce ERG amplitudes.
  2. Visual evoked potentials (VEP): measures the brain’s response to visual signals. Purpose: check the visual pathway beyond the retina, especially if vision is poor after recovery. Mechanism: helps separate retinal from cortical causes (e.g., cortical blindness).

E) Imaging Tests

  1. Color fundus photography (standard or widefield): takes pictures of the retina. Purpose: document whitening, hemorrhages, and vessel color changes over time. Mechanism: allows side‑by‑side comparison as the patient improves.
  2. Optical coherence tomography (OCT, including handheld OCT in children): creates cross‑section “slices” of the retina. Purpose: show swelling or thinning in the inner retina and macula. Mechanism: low blood flow and leak change retinal layers.
  3. Fluorescein angiography (FA): a dye study of retinal blood flow. Purpose: map areas of non‑perfusion and leaking vessels. Mechanism: blocked capillaries appear dark; leaky zones light up.
  4. OCT‑angiography (OCTA): non‑invasive blood‑flow imaging, no dye. Purpose: reveal reduced capillary density in macula and around the optic nerve. Mechanism: shows microvascular damage that matches whitening on exam.

Non-pharmacological treatments

Goal: support life, protect the brain and eyes, and buy time for antimalarials to work.

  1. Immediate ABCs (airway, breathing, circulation) in severe/cerebral malaria; oxygen if hypoxic. Purpose: prevent brain injury. Mechanism: maintains oxygen delivery. PMC

  2. Careful IV fluids (avoid both dehydration and fluid overload). Purpose: correct shock/acid–base problems. Mechanism: restores perfusion without worsening lung/brain edema. WHO Apps

  3. Rapid glucose correction if low. Purpose: prevent seizures/brain injury. Mechanism: reverses neuroglycopenia. CDC Stacks

  4. Seizure first aid and protection from injury; urgent medical treatment follows. Purpose: prevent hypoxia/trauma. Mechanism: safe positioning, airway protection. PMC

  5. Head-up positioning (≈30°) if raised ICP suspected. Purpose: reduce papilledema risk. Mechanism: improves venous outflow. PMC

  6. Temperature control (tepid sponging, fans) alongside antipyretics. Purpose: comfort, reduce metabolic demand. Mechanism: heat loss by conduction/evaporation. PMC

  7. Avoid unnecessary bright light during acute retinal ischemia. Purpose: reduce glare discomfort. Mechanism: less photostress to compromised tissue. (Adjunctive comfort measure.)

  8. Nutrition support (small, frequent feeds as tolerated; enteral nutrition in ICU). Purpose: support recovery. Mechanism: provides energy/protein for healing. PMC

  9. Anemia management with blood transfusion when indicated. Purpose: improve oxygen delivery. Mechanism: raises hemoglobin. CDC

  10. Electrolyte correction (e.g., potassium, sodium). Purpose: prevent arrhythmias/seizures. Mechanism: restores cellular function. PMC

  11. Treat co-infections when suspected (e.g., broad-spectrum antibiotics if sepsis can’t be ruled out). Purpose: reduce overall inflammatory load. Mechanism: eradicates bacterial drivers. European Commission

  12. Gentle fluid strategy if ARDS risk; escalate to ventilatory support when needed. Purpose: protect lungs and brain. Mechanism: avoids fluid-induced pulmonary edema. PMC

  13. Eye protection (lubricants if exposure risk in coma). Purpose: prevent corneal injury. Mechanism: maintains tear film.

  14. Low-vision counseling/rehab after recovery if scotomas/visual field defects persist. Purpose: maximize function. Mechanism: training, magnifiers, lighting optimization.

  15. Regular dilated fundus checks during hospitalization in cerebral malaria. Purpose: track resolution/worsening. Mechanism: serial documentation. PMC

  16. Caregiver education about red flags (vision loss, severe headache, seizures). Purpose: earlier re-presentation.

  17. Avoid harmful “adjuncts” (e.g., routine corticosteroids, mannitol, anti-TNF, exchange transfusion). Purpose: reduce harm. Mechanism: based on evidence of no benefit or harm. European CommissionFrontiersCDC

  18. Early mobilization after stabilization. Purpose: reduce deconditioning.

  19. Psychological support post-ICU (for child and family). Purpose: reduce trauma and improve adherence.

  20. Coordinate follow-up (infectious disease + ophthalmology + neuro/rehab if needed). Purpose: catch delayed hemolysis or visual sequelae early. CDC


Drug treatments

Life-saving rule: In severe malaria, IV artesunate is first-line worldwide, followed by a full oral ACT when you can swallow. In uncomplicated malaria, use an appropriate ACT (choice depends on country guidance). Doses below are typical adult guides; pediatric/pregnancy dosing and local resistance patterns matter.

1) Artesunate (IV) – first-line for severe malaria

  • Class: Artemisinin derivative (parenteral).

  • Dose/time: 2.4 mg/kg IV at 0, 12, 24 h, then daily until oral therapy can be started; children <20 kg often receive 3.0 mg/kg/dose in many programs.

  • Purpose: Rapid parasite clearance and reduced mortality vs quinine.

  • Mechanism: Generates free radicals in parasite, killing blood stages quickly.

  • Key side effects/notes: Monitor for delayed hemolysis for up to 4 weeks; watch LFTs, hemoglobin; transition to oral ACT to complete cure. FDA Access DataOxford Academicseveremalaria.org

2) Artemether–lumefantrine (AL) – oral ACT

  • Class: Artemisinin-based combination therapy.

  • Typical adult dose: Four 20/120 mg tablets per dose: 6 doses over 3 days (0, 8, 24, 36, 48, 60 h); take with food.

  • Use: Uncomplicated falciparum malaria; also as step-down after IV artesunate.

  • Side effects: Nausea, dizziness; drug interactions (CYP). CDCNovartis

3) Dihydroartemisinin–piperaquine (DHA-PQ) – oral ACT

  • Class: ACT (once-daily for 3 days).

  • Use: Uncomplicated malaria (country-specific).

  • Side effects: GI upset; rare QT issues—follow local guidance. WHO Extranetmmv.org

4) Artesunate–amodiaquine (ASAQ) – oral ACT

  • Class: ACT (national program dependent).

  • Note: Follow national dosing schedules. (WHO lists it among recommended ACTs.) PMC

5) Atovaquone–proguanil – oral

  • Class: Mitochondrial inhibitor + DHFR inhibitor combo.

  • Typical adult treatment dose: 4 tablets (1000/400 mg) once daily for 3 days.

  • Use: Uncomplicated malaria; step-down option after IV therapy.

  • Side effects: GI upset; avoid in pregnancy and low-weight infants; interactions with warfarin. CDC

6) Quinine (oral) ± doxycycline/clindamycin

  • Class: Blood schizonticide (quinoline).

  • Use: Alternative where ACTs not available/appropriate; often combined with doxycycline or clindamycin to improve efficacy.

  • Side effects: Cinchonism (tinnitus, headache), hypoglycemia, QT effects. CDC

7) Doxycycline (adjunct)

  • Class: Tetracycline antibiotic (antimalarial partner).

  • Use: Added to quinine in some regimens; not for monotherapy in acute severe malaria because of slow onset.

  • Side effects: Photosensitivity, GI upset; avoid in pregnancy/young children. AAFP

8) Clindamycin (adjunct)

  • Class: Lincosamide (antimalarial partner).

  • Use: Partner with quinine (including in pregnancy when needed) per guidelines.

  • Side effects: Diarrhea, C. difficile risk. CDC

9) Primaquine (single low dose for falciparum transmission blocking; full course for vivax/ovale hypnozoites)

  • Class: 8-aminoquinoline.

  • Use: In certain settings, single dose 0.25 mg/kg added to ACT to reduce falciparum transmission (programmatic decision; check local policy); for P. vivax/ovale, a longer course is used for relapse prevention.

  • Notes: G6PD deficiency matters; pregnancy/infant restrictions apply. World Health OrganizationPMC

10) Antipyretics and anticonvulsants as needed

  • Paracetamol (acetaminophen) for fever/comfort.

  • Benzodiazepines/levetiracetam/phenytoin for seizures (phenobarbital is not first-line due to safety concerns in CM). Frontiers

Not recommended as routine adjuncts: corticosteroids, anti-TNF agents, mannitol, or exchange transfusion—they have not improved outcomes and may cause harm. European CommissionFrontiersCDC


Dietary & supportive supplements

These do not treat malaria. They are supportive for general recovery/eye health. Discuss with your clinician—avoid high doses and interactions.

  1. Oral rehydration solution—small, frequent sips if not vomiting (prevents dehydration).

  2. Protein-rich foods (eggs, lentils, fish) to rebuild during recovery.

  3. Vitamin A (dietary sources; supplement only if deficient). Typical adult RDA ≈ 700–900 mcg RAE/day; avoid excess. Mayo Clinic

  4. Vitamin C (fruits/veg). Aim for diet; adult UL ≈ 2000 mg/day. Mayo Clinic

  5. Vitamin E from foods (nuts/seeds).

  6. Zinc within safe limits (don’t exceed UL without indication). Office of Dietary Supplements

  7. Lutein/zeaxanthin-rich foods (leafy greens, egg yolk). Supplements help AMD patients, not proven for malaria—food first. PubMed

  8. Omega-3 fatty acids (DHA/EPA) from fish; general retinal and neural support. ScienceDirect

  9. B-complex in a standard multivitamin if diet is poor (avoid mega-dosing). Office of Dietary Supplements

  10. Iron only if iron-deficiency anemia is confirmed (doctor-guided).

  11. Folate through foods or standard RDA supplement if needed.

  12. Probiotics/yogurt for gut tolerance during convalescence (evidence general).

  13. Magnesium-rich foods (nuts, legumes, greens).

  14. Antioxidant-rich fruits (berries, citrus) for overall recovery.

  15. Safe sunlight routines + sunglasses (comfort for photophobia).


Regenerative / stem-cell drugs

Short answer: As of 2025, there are no approved immune boosters, regenerative drugs, or stem-cell therapies for malarial retinopathy. Many host-directed “adjuncts” (e.g., anti-TNF, high-dose steroids, mannitol) have failed to improve survival or caused harm in trials of cerebral malaria. Promising lab ideas exist, but not for routine care. If you see claims online, be cautious. BioMed CentralFrontiers


Surgeries

Most patients recover without eye surgery. Rarely, if a complication occurs, retina surgeons may consider:

  1. Pars plana vitrectomy for a non-clearing vitreous hemorrhage or tractional issues obscuring vision.

  2. Laser photocoagulation (PRP) if unusual ischemic neovascular complications appear (very uncommon in malaria, but PRP is the standard for ischemic retinopathies).

  3. Scleral buckle or 4) vitrectomy with laser/gas for a retinal detachment if one occurs.

  4. Cryotherapy/laser retinopexy to seal retinal breaks (if present). EyeWiki+3EyeWiki+3EyeWiki+3


Prevention strategies

  1. Insecticide-treated bed nets (ITNs) every night (newer dual-ingredient nets in resistance areas). CDCWorld Health Organization

  2. Indoor residual spraying (IRS) where available/programmed. World Health Organization

  3. Malaria vaccination for children in eligible countries (RTS,S and R21/Matrix-M per WHO). World Health Organization+1

  4. Chemoprophylaxis for travelers (e.g., atovaquone-proguanil, doxycycline, mefloquine) per destination advice. CDC

  5. Prompt testing and treatment of any fever after exposure. PMC

  6. Window screens, treated curtains, and repellents (DEET, etc.).

  7. Cover up at dusk/dawn (long sleeves, pants).

  8. Community vector control (source reduction).

  9. Prenatal prevention in endemic regions per local policy.

  10. Education on symptoms and early care seeking.


When to see a doctor urgently

  • Any fever after being in (or living in) a malaria area.

  • Confusion, fainting, seizures, severe headache, or coma.

  • Vision suddenly worse, you see dark spots, or severe eye pain.

  • Breathing difficulty, yellow eyes/skin, very dark urine, or severe weakness.

  • In treated severe malaria: return for weekly labs up to 4 weeks to detect delayed hemolysis after IV artesunate. CDC


What to eat—and what to avoid—during recovery

Eat more of:

  1. Fluids (ORS, water, broths) unless your clinician says restrict.

  2. Lean proteins (egg, fish, chicken, lentils).

  3. Leafy greens & colorful veg (lutein/zeaxanthin, vitamin C). Office of Dietary Supplements

  4. Whole grains for steady energy.

  5. Fruits (citrus, berries, guava) for vitamin C and antioxidants. Mayo Clinic

Limit/avoid:

  1. Alcohol (dehydrates, stresses liver).

  2. Very fatty, spicy, or heavy meals while nauseated.

  3. Mega-dose supplements unless prescribed (watch ULs). Office of Dietary Supplements

  4. Unpasteurized/unsafe foods (infection risk).

  5. Smoking (worsens vascular health).


FAQs

1) Can malarial retinopathy cause permanent blindness?
Usually no, especially if treated promptly; many changes improve as the malaria clears. Severe cases can leave scotomas or other defects. ajtmh.org

2) Does everyone with malaria get these eye changes?
No. They’re most common in cerebral/severe falciparum malaria, especially in children. PMC

3) How do doctors confirm it?
By dilated eye exam; sometimes with fundus photos, FA, or OCT for detail. PMC

4) Is the retina damage the same as brain damage?
They’re closely related—the same small-vessel process happens in both. The retina helps doctors judge severity. PMC

5) What is the fastest life-saving treatment?
IV artesunate for severe malaria, followed by a full oral ACT. FDA Access Data

6) Are steroids, mannitol, or anti-TNF helpful?
No—not recommended; trials show no benefit and possible harm. European CommissionFrontiers

7) Is exchange transfusion useful?
No—CDC no longer recommends it for severe malaria. CDC

8) If I had IV artesunate, do I need more checks?
Yes—weekly labs up to 4 weeks to watch for delayed hemolysis. CDC

9) Can supplements cure malarial retinopathy?
No. They’re supportive only; antimalarials do the curing. CDC

10) Will I need eye surgery?
Almost never. Surgery is only for rare complications like a non-clearing vitreous hemorrhage or retinal detachment. EyeWiki

11) Do children need vaccines against malaria?
In eligible countries, RTS,S and R21 vaccines are WHO-recommended for children to prevent malaria. World Health Organization

12) How long until vision feels normal?
Often days to weeks as the systemic illness resolves, but persistent spots can remain if ischemia was severe. Follow-up helps track recovery. ajtmh.org

13) What if my rapid test is negative?
Ask for blood smears; they’re the gold standard and also quantify parasite load. emDocs

14) Which oral ACT is “best”?
Depends on local guidelines and resistance. Common choices: AL or DHA-PQ; your clinician will choose. CDCWHO Extranet

15) Can I prevent this if I live in an endemic area?
Use ITNs, IRS where offered, seek testing early for fever, and follow local preventive programs (including vaccination for children). World Health Organization+1


Disclaimer: Each person’s journey is unique, treatment planlife stylefood habithormonal conditionimmune systemchronic 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 11, 2025.

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