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.
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
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
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
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.
