This document discusses choroiditis, an inflammation of the choroid layer of the eye. It begins by introducing choroiditis and classifying it anatomically and by etiology. It then discusses infectious causes such as parasites, bacteria, viruses, and fungi. Non-infectious causes are also listed. The document outlines symptoms, signs, and characteristics of choroiditis lesions. Specific sections provide details on toxoplasmosis and toxocariasis, two common causes of choroiditis. Treatment options including medications, surgery, and procedures are mentioned. In summary, the document provides a comprehensive overview of choroiditis, including causes, presentation, diagnosis, and management.

1. Dr. Samarth Mishra
CHOROIDITIS

2. INTRODUCTION
• Inflammation of
choroid; associated
with the highest risk
of severe vision loss.
(Standardization of
Uveitis Nomenclature
(SUN) Working
Group)
• Always Involving
retina, Retinal
vessels, optic nerve
head.

3. CLASSIFICATION
 ANATOMICAL –
 Choroiditis
 Chorioretinitis
 Retinochoroiditis
 Neuro-uveitis
 AETIOLOGICAL – infective/non-infective

4. INFECTIOUS
1. Parasitic
 – Toxoplasmosis
 – Toxocariasis
 – Onchocerciasis
 – Cysticercosis
2. Bacterial –
 - tuberculosis
 - syphilis
3. Viral
– Herpes viruses
• ARN
• CMV retinitis
 Epstein-Barr virus
– Rubella
– Rubeola (measles)
– West Nile virus

5. 3. Fungal
 – Candidiasis
 – Aspergillosis
 – Cryptococcosis
 – Coccidioidomycosis

6. NON-INFECTIOUS CAUSE
 Multifocal Choroiditis
and Panuveitis
 Punctate Inner
Choroidopathy
 Subretinal Fibrosis
and Uveitis
 Serpiginous
choroidopathy
 Acute retinal pigment
epitheliitis
 Birdshot
choroidopathy
 􀁺 Retinal Vasculitis
 – Behcets
 – SLE
 – Wegeners
granulomatosis
 – PAN
 – Eales disease
 – Frosted-branch
angiitis

7. SYMPTOMS
 Floaters
 Impaired central vision ( pain or painless )
 Pain, redness & photophobia if associated
with ant. Segment involvement
 Metamorphopsia, micro/macropsia
 Perception of black spot

8. SIGNS –
 Inflammatory cells & vitritis
 Exudates, Edema & infiltrations in
retina / choroid
 Sheathing of vessels
Other signs –
 Disc edema
 Retinal haemorrhages
 Spill-over uveitis
 Complicated cataract
 Glaucoma
 RD
 Choroid neovascularisation

9. CHOROIDITIS
 Focal / multifocal /diffuse/central/ juxtapapillary
 Granulomatous or non-granulomatous/ exudative
choroiditis
 Ophthalmoscopic picture –
1 . Active lesion – early stage - yellowish area with hazy
edges & ill defined margin due to infiltration & exudation , lie
deeper to retinal vessels
- Late stage – bruch’s membrane destroyed – infiltration of
leukocytes to retina & vitreous
↓
organisation of exudation due to fibroblastic activity of stroma
↓
Firm fusion of retina & choroid due to destruction of normal
structure by fibrous tissue

10.  Old choroiditis lesion –
- White colour lesion due to fibrous tissue deposition, thinning &
atrophy – white reflex from sclera
 Surrounded by black zone of pigment from RPE
 RETINITIS - Focal /multifocal / geographic /diffuse
 Active lesions – whitis retinal opacities with indistinct boarder due to
surronding edema
 Later on boarder become well defined
VASCULITIS –
 Periphlebitis > periarteritis
 Active vasculitis – yellowish/grey-white, patchy perivascular
sheathing, with haemorrhage

11. TOXOPLASMOSIS
 Most common cause of choroiditis in immuno
competent patient.
 Intraocular infection is often accompanied by
CNS involvement in immuno compromised
patient.
 Caused by toxoplasma gondii.
 Infest >10% of adults in northern temperate
countries & > 50% of adults in
mediterranean & tropical countries.

12.  Three forms of the parasite:
- tachyzoite ( trophozoite) – invassive form
responsible for acute infection,
- bradyzoite ( tissue cyst) – latent or recurent
infection
- sporozoite (oocyst).
 MODE OF INFECTION
 Ingestion of undercooked meat containing bradyzoites.
 Ingestion of oocyst from contaminated hand, food or
water.
 Transplacental – 40% of fetus is affected if mother is
infected during pregnancy.

13. PATHOGENESIS
 Clinically, the infestation starts as a focal area of
retinitis, with an overlying vitritis.
 Atypical, severe toxoplasmic retinochoroiditis in the
elderly can mimic ARN.
 zonal granuloma with intense central necrosis
surrounded by successive layers of mononuclear
cells - ↑ed Plasma cells at periphery → secrete
antibodies → destruction of the free parasites in the
extracellular space → cyst formation by parasites
 Proliferation of the RPE cells, and healing of the
lesion is associated with scar formation

14. HISTOLOGY
 Found in three forms: free, pseudocysts, or in true
cysts.
a. Rarely, the protozoa may be found in a free form in
the neural retina.
b. Multiplies in the confines of the cell membrane→ a
group of protozoa surrounded by the retinal cell
membrane→ pseudocyst
C. If environment becomes inhospitable, an Intracellular
protozoan (trophozoite) may transform into bradyzoite,
surround itself with a self-made membrane, multiply,
and then form a true cyst.

15. CLINICAL MANIFESTATION OF
TOXOPLASMOSIS
 The most frequent form of infection with T. gondii
is subclinical, and is discovered by serologic
testing for antibodies to Toxoplasma organisms.
 clinical entities of toxoplasmosis:
- congenital toxoplasmosis
- acquired systemic toxoplasmosis
- toxoplasmosis in the immunocompromised host
- acquired or reactivation of a latent infection

16. CONGENITAL TOXOPLASMOSIS
 Results from transplacental transmission of T. gondii.
 Incidence of congenital infection varies with the trimester
during which the mother becomes infected.
 lowest incidence occurs in the first trimester (15% to
20%), and highest incidence in the third trimester (59%).
 If infection occurs in – 1st trimester → spontaneous
abortion
- 3rd trimester → subclinical
infection

17. COURSE OF DISEASE:-
 Healing of the retinitis is associated with a decrease
in retinal edema and flattening of the lesion with
evidence of scar formation surrounded by variable
amounts of pigment .
 lesion may appear as a punched out scar with
underlying sclera resulting from extensive retinal and
choroidal necrosis surrounded by pigment
proliferation , it may become a conglomerate or
proliferated retinal pigment cells, or it may be small
and appear as a pigment clump in the retina.

18. OCULAR MANIFESTATION
 Ocular findings include involvement of the retina,
choroid, retinal vessels, macula, optic nerve,
vitreous, and anterior uvea.
 TYPICAL –
-Focus of retinitis surrounded by fuzzy retinal
edema
-Pigmented atrophic retinochoroiditic scar
-Vitreous cells and exudates
-Focal retinal vasculitis
-Hyperemia of optic nerve head
-Cells and flare in the anterior chamber

19.  Atypical Manifestations:-
Juxtapapillar retinitis
Retrobulbar neuritis
Rhegmatogenous RD
Pars planitis
Punctate outer retinitis
Serous macular detachment
BRAO/BRVO
Retinal or subretinal neovascularization
Choroidoretinal vascular anastomosis
Panuveitis

20. Toxoplasmic retinitis – focus of necrotising retinitis
surrounded by retinal edema, retinal vasculitis.
- Solitary inflammatory focus near an old pigmented scar.
( satelite lesion )
- Severe vitritis impairing visualisation of fundus →
HEADLIGHT IN FOG
appearance.
-In immunocompromised – multifocal retinal lesion often B/L,
less vitritis - simulate ARN.
- There may be sec. nongranulomatous inflammation of choroid
& sclera.
- When choroid is involved called as
retinochoroiditis.

21.  Occurs in 3 morphological variants :-
1. In most severe disease – lesion of > 1 DD, dense &
elevated lesion, & are largely destructive.
- assosiated with severe vitritis & ant. Chamber
reaction.
- Prompt therapy is needed regardless of site of lesion.
2. 2nd variant :- punctate lesion of inner retina, mild
inflammation, no therapy needed unless the lesion is
close to macula.
3. 3rd variant :- punctate lesion in outer retina with mild
vitritis, spontaneous resolution

22. OPTIC NERVE
optic neuritis or papillitis associated with edema, Later
Juxtapapillary Retinochoroiditis and Macular Star
develop.
VITREOUS
-Posterior vitreous detachment common
-precipitates of inflammatory cells on the posterior vitreous
face
 ANTERIOR UVEA
- Anterior uveitis (granulomatous or nongranulomatous)
may be associated with Toxoplasma retinochoroiditis

23. COMPLICATIONS
 Posterior synaechiae
 Macular edema
 Dragging of macula
 RD
 Choroidal neovascularisation
 BRAO/BRVO
 Optic atrophy
 Cataract
 Glaucoma
 u/l pigmentary retinopathy

24. DIAGNOSIS
 Classic fundus finding
 Serological testing –
- Sabin-Feldman dye test, ELISA, IFA test, IHA
test, agglutination test.
 PCR in vitreous sample
 Isolation of organism from aquous, vitreous
 CNS imaging
 Fluorescein angiographic - presence a dark
hypofluorescent center of the lesion surrounded by an area of
hyperfluorescence.
 ICG
 OCT, USG

25. TREATMENT
 Pyrimethamine: Loading dose: 100 mg (1st day), followed by 25 mg
once daily +
Sulfadiazine: 4 Gr daily divided in every 6 hours For 4 to 6 weeks.
 Oral corticosteroids must be initiated at least 24 hours after starting anti
parasitic drugs.
 Folinic acid also given
Other drugs used in various combinations include:
 Clindamycin, Trimethoprim + Sulphamethoxazol (Co-Trimoxazole),
Spiramycin, Azithromycin
 Therapy regimens used during Pregnancy: Spiramycin- 2 gr/day in two
divided doses
 Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinic
acid

26.  SURGICAL T/t –
- Pars Plana Vitrectomy: to remove Vitreous
Opacities, or to relieve the persistent Vitreo-Retinal
traction.
- Scleral Buckling: in cases complicated with
Retinal Detachment.
 PHOTOCOAGULATION AND CRYOTHERAPY
- Both photocoagulation and cryotherapy cause
destruction of the Toxoplasma cyst and the
tachyzoites in the retina

27. TOXOCARIASIS
 Toxocara canis: nematode
 Dog primary host
 Children who have pica, close contact with
Puppies.
 Unilateral, Male > female, Children, young adults
 DDx of leukocoria (r/o RB)
􀁺 Ova ingested
 – Visceral larva migrans
 – Larvae encyst in tissues
 – Never mature in humans – no ova in stool

28. CLINICAL FEATURES
1. Granuloma in the Peripheral Retina and
Vitreous.
2. Posterior Pole Granuloma.
3. Chronic Endophthalmitis.

29. DIAGNOSIS
 Anti-Toxocara antibodies
– Any serum titer significant
– Higher titer in aqueous
 Eosinophils in aqueous/vitreous
TREATMENT
 Medical treatment is directed toward the inflammatory
response that produces Structural Damage and
decreased vision - with Topical or Systemic Steroids.
 Antihelminthic therapy for Ocular Toxocariasis do not
alter natural course of the disease

30.  Cysticercosis
- South/Central America, Africa, Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
 Treatment: vitrectomy for subretinal cysticercus
 Onchocerciasis
 River blindness” - blackflies
 Microfilariae in cornea, aqueous; skin nodules
 Attenuated vessels, perivascular sheathing, RPE atrophy;
optic atrophy late
 Ivermectin 150 mic/kg q year x 10 years

31. TUBERCULOUS UVEITIS
 The most common presentation is disseminated
choroiditis.
 Deep in the choroid, appear yellow, white, or
gray, and are fairly well circumscribed.
 Vast majority of cases, the lesions present in the
posterior pole.
 single tubercle, focal choroiditis,which can occur
at the posterior pole, typically elevated and may
be accompanied by an overlying serous retinal
detachment
 Subretinal abscess is formed progressively from a
choroidal tubercle, which can be single or
multiple.
 Periphlebitis often b/l

32. SYPHILITIC UVEITIS present as chorioretinitis, neuroretinitis, salt-pepper
retinopathy, optic neuritis, papilloedema, and optic
perineuritis.
 Syphilis can present with placoid choroidal lesions.
 Unusual manifestation of syphilis is acute
necrotizing retinopathy, which mimics ARN.
 In HIV-positive patients, ocular syphilis is more
closely associated with neurological abnormalities

33. Rubella
Congenital
– Ocular involvement increased if contracted during 1st
trimester
– Cataract - retention of cell nuclei in embryonic
nucleus
– Chronic nongranulomatous iritis; iris atrophy
- “Salt-and-pepper” fundus – vision, ERG unaffected
 – Choroidal neovascularization rare complication
Acquired
– German measles
– Conjunctivitis, keratitis, iritis, bilateral retinitis with

34. Measles (Rubeola)
􀁺 Congenital
– “Salt-and-pepper” fundus
􀁺 Acquired
– Macular edema, neuroretinitis, attenuated vessels
􀁺 Subacute sclerosing panencephalitis (SSPE)
– Slow virus - mutation of measles virus
– Encephalitis with progressive deficits
– Disc edema, optic atrophy, macular
- infiltrate/hemorrhage/gliosis
– Supportive treatment; poor prognosis

35. West Nile Virus
 Creamy target like chorioretinal lesions, 300 – 1000
μm, scattered diffusely
 Hypofluorescent centrally and hyperfluorescent
edges
 Multifocal chorioretinitis
– Vitritis, iridocyclitis
– Occlusive retinal vasculitis - multiple branch artery
occlusions
– Optic nerve: optic neuritis, mild disc edema
􀁺 Congenital - chorioretinal scarring

36. FUNGAL UVEITIS

37. Ocular Histoplasmosis/ presumed
occular histoplasmosis syndrome
 Histoplasma capsulatum
 20 – 50 yr, HLA-B7 – associated with macular lesions
 Punched-out CR scars (“histo spots”)
 Peripapillary atrophy, Macular scar, No vitreous cells
 FA -
– Active choroiditis: early hypofluorescence with late staining
– CNV: early hyperfluorescence with late leakage

38. Treatment -
– Extrafoveal CNV: photocoagulation
- Juxtafoveal CNV: photocoagulation
 – Risk of CNV in fellow eye with histo spot in
macula: 25% @ 3 years
 SF CNV-
 Photodynamic therapy/ Steroids/Anti-VEGF/
Combination
 Subfoveal surgery- benefit for POHS if < 20/100

39. Candidiasis
 Immunosuppressed patients, indwelling catheters,
hyperalimentation
 Incidence of endophthalmitis in candidemia
– No antifungal treatment – 10 – 37%
– On antifungal treatment – 3%
 Choroidal infection with secondary retinal,
 vitreous involvement – fluffy yellow lesions
 Treatment
– IV, periocular, intravitreal antifungals (amphotericin B,
ketoconazole)
– Consider vitrectomy if significant vitritis

40. NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS & PANUVEITIS (
MCP )
􀁺 Female > male
􀁺 “Pseudo-POHS” – histo spots
􀁺 Vitritis, +/- anterior uveitis
􀁺 Macular CNV in 1/3
􀁺 FA: Early hyperfluorescence with late staining
􀁺 Diagnosis of exclusion- TB, syphilis, sarcoidosis,
􀁺 Treatment
– Steroids – Local/ Systemic
– Other immunosuppressives

41.  Punctate Inner Choroidopathy (PIC)
- Subgroup of MCP
- Young, female, myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid & retina
- 40 % dev. CNV
 Subretinal fibrosis and uveitis
-Young, female, African-American, bilateral
- Chronic vitritis, CME
- Gliotic yellow-white subretinal lesions, gradually coalesce
- Poor prognosis
- Corticosteroids (esp for CME)
– other immunosuppressives

42. Serpiginous Choroidopathy
(geographic, helicoid)
 Adults; usually bilateral, Yellow-gray lesions
 Start from optic nerve, progress centrifugally
 Active lesions adjacent to scarred inactive area
 Mild vitritis, NVD, CNV
 FA
– Early in disease – like AMPPE
– Later in disease – window defects
 Steroids, other immunosuppressives
 Poor prognosis

43. Birdshot Retinochoroidopathy (BSRC)
 Vitiliginous choroiditis
 Females > males, 30 – 70 years old
 Symptoms:
Painless Visual Loss
Floaters,
Photophobia,
Nyctalopia, and Disturbances in Color Vision.
 Scattered round or oval cream-colored spots, May become Confluent resulting in larger
Geographic areas of Hypopigmentation.
 CME
 Vitritis
 Disc edema
 Arteriolar narrowing

44.  FA
– Retinal lesions often silent
 – CME, periphlebitis
Diagnostic
– HLA-A29 - 50-80% birdshot
 ERG may be reduced
Treatment
 – Corticosteroids – may help in ~ 50%
 – immunosuppressives - Mycophenolate,
Cyclosporine
• Quiescent 2 yrs then slow taper

45. CONCLUSION
 Choroiditis entities have very characteristic
clinical features and diagnosis is mainly clinical.
 Essential to differentiate infective and non-
infective conditions as their management is
diametrically opposite.
 Empirical use of systemic steroids or
immunosuppressives in all cases of Choroiditis
should be absolutely avoided.
 Follow-up all patients with Choroiditis even after
the resolution of lesions for complications related
to the disease.

46. THANK YOU