Embed Size (px)
Citation preview
Dr Samarth Mishra
CHOROIDITIS
INTRODUCTIONbull Inflammation of
choroid associated
with the highest risk
of severe vision loss
(Standardization of
Uveitis Nomenclature
(SUN) Working
Group)
bull Always Involving
retina Retinal
vessels optic nerve
head
CLASSIFICATION
ANATOMICAL ndash
Choroiditis
Chorioretinitis
Retinochoroiditis
Neuro-uveitis
AETIOLOGICAL ndash infectivenon-infective
INFECTIOUS
1 Parasitic
ndash Toxoplasmosis
ndash Toxocariasis
ndash Onchocerciasis
ndash Cysticercosis
2 Bacterial ndash
- tuberculosis
- syphilis
3 Viral
ndash Herpes viruses
bull ARN
bull CMV retinitis
Epstein-Barr virus
ndash Rubella
ndash Rubeola (measles)
ndash West Nile virus
3 Fungal
ndash Candidiasis
ndash Aspergillosis
ndash Cryptococcosis
ndash Coccidioidomycosis
NON-INFECTIOUS CAUSE
Multifocal Choroiditis
and Panuveitis
Punctate Inner
Choroidopathy
Subretinal Fibrosis
and Uveitis
Serpiginous
choroidopathy
Acute retinal pigment
epitheliitis
Birdshot
choroidopathy
1048698 Retinal Vasculitis
ndash Behcets
ndash SLE
ndash Wegeners
granulomatosis
ndash PAN
ndash Eales disease
ndash Frosted-branch
angiitis
SYMPTOMS
Floaters
Impaired central vision ( pain or painless )
Pain redness amp photophobia if associated
with ant Segment involvement
Metamorphopsia micromacropsia
Perception of black spot
SIGNS ndash
Inflammatory cells amp vitritis
Exudates Edema amp infiltrations in
retina choroid
Sheathing of vessels
Other signs ndash
Disc edema
Retinal haemorrhages
Spill-over uveitis
Complicated cataract
Glaucoma
RD
Choroid neovascularisation
CHOROIDITIS Focal multifocal diffusecentral juxtapapillary
Granulomatous or non-granulomatous exudative choroiditis
Ophthalmoscopic picture ndash
1 Active lesion ndash early stage - yellowish area with hazy edges amp ill defined margin due to infiltration amp exudation lie deeper to retinal vessels
- Late stage ndash bruchrsquos membrane destroyed ndash infiltration of leukocytes to retina amp vitreous
darr
organisation of exudation due to fibroblastic activity of stroma
darr
Firm fusion of retina amp choroid due to destruction of normal structure by fibrous tissue
Old choroiditis lesion ndash
- White colour lesion due to fibrous tissue deposition thinning amp atrophy ndash white reflex from sclera
Surrounded by black zone of pigment from RPE
RETINITIS - Focal multifocal geographic diffuse
Active lesions ndash whitis retinal opacities with indistinct boarder due to surronding edema
Later on boarder become well defined
VASCULITIS ndash Periphlebitis gt periarteritis
Active vasculitis ndash yellowishgrey-white patchy perivascular sheathing with haemorrhage
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 gt10 of adults in northern temperate
countries amp gt 50 of adults in
mediterranean amp tropical countries
Three forms of the parasite
- tachyzoite ( trophozoite) ndash invassive form responsible for acute infection
- bradyzoite ( tissue cyst) ndash latent or recurentinfection
- sporozoite (oocyst)
MODE OF INFECTION
Ingestion of undercooked meat containing bradyzoites
Ingestion of oocyst from contaminated hand food or water
Transplacental ndash 40 of fetus is affected if mother is infected during pregnancy
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 - uarred Plasma cells at periphery rarr secrete
antibodies rarr destruction of the free parasites in the
extracellular space rarr cyst formation by parasites
Proliferation of the RPE cells and healing of the
lesion is associated with scar formation
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 membranerarr a
group of protozoa surrounded by the retinal cell
membranerarr 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
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
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 ndash 1st trimester rarr spontaneous abortion
- 3rd trimester rarr subclinical infection
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
OCULAR MANIFESTATION
Ocular findings include involvement of the retina
choroid retinal vessels macula optic nerve
vitreous and anterior uvea
TYPICAL ndash
-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
Atypical Manifestations-Juxtapapillar retinitis
Retrobulbar neuritis
Rhegmatogenous RD
Pars planitis
Punctate outer retinitis
Serous macular detachment
BRAOBRVO
Retinal or subretinal neovascularization
Choroidoretinal vascular anastomosis
Panuveitis
Toxoplasmic retinitis ndash 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 rarr HEADLIGHT IN FOG
appearance
-In immunocompromised ndash multifocal retinal lesion often BL less vitritis - simulate ARN
- There may be sec nongranulomatous inflammation of choroid amp sclera
- When choroid is involved called as retinochoroiditis
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
INTRODUCTIONbull Inflammation of
choroid associated
with the highest risk
of severe vision loss
(Standardization of
Uveitis Nomenclature
(SUN) Working
Group)
bull Always Involving
retina Retinal
vessels optic nerve
head
CLASSIFICATION
ANATOMICAL ndash
Choroiditis
Chorioretinitis
Retinochoroiditis
Neuro-uveitis
AETIOLOGICAL ndash infectivenon-infective
INFECTIOUS
1 Parasitic
ndash Toxoplasmosis
ndash Toxocariasis
ndash Onchocerciasis
ndash Cysticercosis
2 Bacterial ndash
- tuberculosis
- syphilis
3 Viral
ndash Herpes viruses
bull ARN
bull CMV retinitis
Epstein-Barr virus
ndash Rubella
ndash Rubeola (measles)
ndash West Nile virus
3 Fungal
ndash Candidiasis
ndash Aspergillosis
ndash Cryptococcosis
ndash Coccidioidomycosis
NON-INFECTIOUS CAUSE
Multifocal Choroiditis
and Panuveitis
Punctate Inner
Choroidopathy
Subretinal Fibrosis
and Uveitis
Serpiginous
choroidopathy
Acute retinal pigment
epitheliitis
Birdshot
choroidopathy
1048698 Retinal Vasculitis
ndash Behcets
ndash SLE
ndash Wegeners
granulomatosis
ndash PAN
ndash Eales disease
ndash Frosted-branch
angiitis
SYMPTOMS
Floaters
Impaired central vision ( pain or painless )
Pain redness amp photophobia if associated
with ant Segment involvement
Metamorphopsia micromacropsia
Perception of black spot
SIGNS ndash
Inflammatory cells amp vitritis
Exudates Edema amp infiltrations in
retina choroid
Sheathing of vessels
Other signs ndash
Disc edema
Retinal haemorrhages
Spill-over uveitis
Complicated cataract
Glaucoma
RD
Choroid neovascularisation
CHOROIDITIS Focal multifocal diffusecentral juxtapapillary
Granulomatous or non-granulomatous exudative choroiditis
Ophthalmoscopic picture ndash
1 Active lesion ndash early stage - yellowish area with hazy edges amp ill defined margin due to infiltration amp exudation lie deeper to retinal vessels
- Late stage ndash bruchrsquos membrane destroyed ndash infiltration of leukocytes to retina amp vitreous
darr
organisation of exudation due to fibroblastic activity of stroma
darr
Firm fusion of retina amp choroid due to destruction of normal structure by fibrous tissue
Old choroiditis lesion ndash
- White colour lesion due to fibrous tissue deposition thinning amp atrophy ndash white reflex from sclera
Surrounded by black zone of pigment from RPE
RETINITIS - Focal multifocal geographic diffuse
Active lesions ndash whitis retinal opacities with indistinct boarder due to surronding edema
Later on boarder become well defined
VASCULITIS ndash Periphlebitis gt periarteritis
Active vasculitis ndash yellowishgrey-white patchy perivascular sheathing with haemorrhage
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 gt10 of adults in northern temperate
countries amp gt 50 of adults in
mediterranean amp tropical countries
Three forms of the parasite
- tachyzoite ( trophozoite) ndash invassive form responsible for acute infection
- bradyzoite ( tissue cyst) ndash latent or recurentinfection
- sporozoite (oocyst)
MODE OF INFECTION
Ingestion of undercooked meat containing bradyzoites
Ingestion of oocyst from contaminated hand food or water
Transplacental ndash 40 of fetus is affected if mother is infected during pregnancy
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 - uarred Plasma cells at periphery rarr secrete
antibodies rarr destruction of the free parasites in the
extracellular space rarr cyst formation by parasites
Proliferation of the RPE cells and healing of the
lesion is associated with scar formation
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 membranerarr a
group of protozoa surrounded by the retinal cell
membranerarr 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
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
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 ndash 1st trimester rarr spontaneous abortion
- 3rd trimester rarr subclinical infection
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
OCULAR MANIFESTATION
Ocular findings include involvement of the retina
choroid retinal vessels macula optic nerve
vitreous and anterior uvea
TYPICAL ndash
-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
Atypical Manifestations-Juxtapapillar retinitis
Retrobulbar neuritis
Rhegmatogenous RD
Pars planitis
Punctate outer retinitis
Serous macular detachment
BRAOBRVO
Retinal or subretinal neovascularization
Choroidoretinal vascular anastomosis
Panuveitis
Toxoplasmic retinitis ndash 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 rarr HEADLIGHT IN FOG
appearance
-In immunocompromised ndash multifocal retinal lesion often BL less vitritis - simulate ARN
- There may be sec nongranulomatous inflammation of choroid amp sclera
- When choroid is involved called as retinochoroiditis
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
CLASSIFICATION
ANATOMICAL ndash
Choroiditis
Chorioretinitis
Retinochoroiditis
Neuro-uveitis
AETIOLOGICAL ndash infectivenon-infective
INFECTIOUS
1 Parasitic
ndash Toxoplasmosis
ndash Toxocariasis
ndash Onchocerciasis
ndash Cysticercosis
2 Bacterial ndash
- tuberculosis
- syphilis
3 Viral
ndash Herpes viruses
bull ARN
bull CMV retinitis
Epstein-Barr virus
ndash Rubella
ndash Rubeola (measles)
ndash West Nile virus
3 Fungal
ndash Candidiasis
ndash Aspergillosis
ndash Cryptococcosis
ndash Coccidioidomycosis
NON-INFECTIOUS CAUSE
Multifocal Choroiditis
and Panuveitis
Punctate Inner
Choroidopathy
Subretinal Fibrosis
and Uveitis
Serpiginous
choroidopathy
Acute retinal pigment
epitheliitis
Birdshot
choroidopathy
1048698 Retinal Vasculitis
ndash Behcets
ndash SLE
ndash Wegeners
granulomatosis
ndash PAN
ndash Eales disease
ndash Frosted-branch
angiitis
SYMPTOMS
Floaters
Impaired central vision ( pain or painless )
Pain redness amp photophobia if associated
with ant Segment involvement
Metamorphopsia micromacropsia
Perception of black spot
SIGNS ndash
Inflammatory cells amp vitritis
Exudates Edema amp infiltrations in
retina choroid
Sheathing of vessels
Other signs ndash
Disc edema
Retinal haemorrhages
Spill-over uveitis
Complicated cataract
Glaucoma
RD
Choroid neovascularisation
CHOROIDITIS Focal multifocal diffusecentral juxtapapillary
Granulomatous or non-granulomatous exudative choroiditis
Ophthalmoscopic picture ndash
1 Active lesion ndash early stage - yellowish area with hazy edges amp ill defined margin due to infiltration amp exudation lie deeper to retinal vessels
- Late stage ndash bruchrsquos membrane destroyed ndash infiltration of leukocytes to retina amp vitreous
darr
organisation of exudation due to fibroblastic activity of stroma
darr
Firm fusion of retina amp choroid due to destruction of normal structure by fibrous tissue
Old choroiditis lesion ndash
- White colour lesion due to fibrous tissue deposition thinning amp atrophy ndash white reflex from sclera
Surrounded by black zone of pigment from RPE
RETINITIS - Focal multifocal geographic diffuse
Active lesions ndash whitis retinal opacities with indistinct boarder due to surronding edema
Later on boarder become well defined
VASCULITIS ndash Periphlebitis gt periarteritis
Active vasculitis ndash yellowishgrey-white patchy perivascular sheathing with haemorrhage
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 gt10 of adults in northern temperate
countries amp gt 50 of adults in
mediterranean amp tropical countries
Three forms of the parasite
- tachyzoite ( trophozoite) ndash invassive form responsible for acute infection
- bradyzoite ( tissue cyst) ndash latent or recurentinfection
- sporozoite (oocyst)
MODE OF INFECTION
Ingestion of undercooked meat containing bradyzoites
Ingestion of oocyst from contaminated hand food or water
Transplacental ndash 40 of fetus is affected if mother is infected during pregnancy
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 - uarred Plasma cells at periphery rarr secrete
antibodies rarr destruction of the free parasites in the
extracellular space rarr cyst formation by parasites
Proliferation of the RPE cells and healing of the
lesion is associated with scar formation
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 membranerarr a
group of protozoa surrounded by the retinal cell
membranerarr 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
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
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 ndash 1st trimester rarr spontaneous abortion
- 3rd trimester rarr subclinical infection
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
OCULAR MANIFESTATION
Ocular findings include involvement of the retina
choroid retinal vessels macula optic nerve
vitreous and anterior uvea
TYPICAL ndash
-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
Atypical Manifestations-Juxtapapillar retinitis
Retrobulbar neuritis
Rhegmatogenous RD
Pars planitis
Punctate outer retinitis
Serous macular detachment
BRAOBRVO
Retinal or subretinal neovascularization
Choroidoretinal vascular anastomosis
Panuveitis
Toxoplasmic retinitis ndash 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 rarr HEADLIGHT IN FOG
appearance
-In immunocompromised ndash multifocal retinal lesion often BL less vitritis - simulate ARN
- There may be sec nongranulomatous inflammation of choroid amp sclera
- When choroid is involved called as retinochoroiditis
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
INFECTIOUS
1 Parasitic
ndash Toxoplasmosis
ndash Toxocariasis
ndash Onchocerciasis
ndash Cysticercosis
2 Bacterial ndash
- tuberculosis
- syphilis
3 Viral
ndash Herpes viruses
bull ARN
bull CMV retinitis
Epstein-Barr virus
ndash Rubella
ndash Rubeola (measles)
ndash West Nile virus
3 Fungal
ndash Candidiasis
ndash Aspergillosis
ndash Cryptococcosis
ndash Coccidioidomycosis
NON-INFECTIOUS CAUSE
Multifocal Choroiditis
and Panuveitis
Punctate Inner
Choroidopathy
Subretinal Fibrosis
and Uveitis
Serpiginous
choroidopathy
Acute retinal pigment
epitheliitis
Birdshot
choroidopathy
1048698 Retinal Vasculitis
ndash Behcets
ndash SLE
ndash Wegeners
granulomatosis
ndash PAN
ndash Eales disease
ndash Frosted-branch
angiitis
SYMPTOMS
Floaters
Impaired central vision ( pain or painless )
Pain redness amp photophobia if associated
with ant Segment involvement
Metamorphopsia micromacropsia
Perception of black spot
SIGNS ndash
Inflammatory cells amp vitritis
Exudates Edema amp infiltrations in
retina choroid
Sheathing of vessels
Other signs ndash
Disc edema
Retinal haemorrhages
Spill-over uveitis
Complicated cataract
Glaucoma
RD
Choroid neovascularisation
CHOROIDITIS Focal multifocal diffusecentral juxtapapillary
Granulomatous or non-granulomatous exudative choroiditis
Ophthalmoscopic picture ndash
1 Active lesion ndash early stage - yellowish area with hazy edges amp ill defined margin due to infiltration amp exudation lie deeper to retinal vessels
- Late stage ndash bruchrsquos membrane destroyed ndash infiltration of leukocytes to retina amp vitreous
darr
organisation of exudation due to fibroblastic activity of stroma
darr
Firm fusion of retina amp choroid due to destruction of normal structure by fibrous tissue
Old choroiditis lesion ndash
- White colour lesion due to fibrous tissue deposition thinning amp atrophy ndash white reflex from sclera
Surrounded by black zone of pigment from RPE
RETINITIS - Focal multifocal geographic diffuse
Active lesions ndash whitis retinal opacities with indistinct boarder due to surronding edema
Later on boarder become well defined
VASCULITIS ndash Periphlebitis gt periarteritis
Active vasculitis ndash yellowishgrey-white patchy perivascular sheathing with haemorrhage
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 gt10 of adults in northern temperate
countries amp gt 50 of adults in
mediterranean amp tropical countries
Three forms of the parasite
- tachyzoite ( trophozoite) ndash invassive form responsible for acute infection
- bradyzoite ( tissue cyst) ndash latent or recurentinfection
- sporozoite (oocyst)
MODE OF INFECTION
Ingestion of undercooked meat containing bradyzoites
Ingestion of oocyst from contaminated hand food or water
Transplacental ndash 40 of fetus is affected if mother is infected during pregnancy
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 - uarred Plasma cells at periphery rarr secrete
antibodies rarr destruction of the free parasites in the
extracellular space rarr cyst formation by parasites
Proliferation of the RPE cells and healing of the
lesion is associated with scar formation
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 membranerarr a
group of protozoa surrounded by the retinal cell
membranerarr 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
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
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 ndash 1st trimester rarr spontaneous abortion
- 3rd trimester rarr subclinical infection
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
OCULAR MANIFESTATION
Ocular findings include involvement of the retina
choroid retinal vessels macula optic nerve
vitreous and anterior uvea
TYPICAL ndash
-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
Atypical Manifestations-Juxtapapillar retinitis
Retrobulbar neuritis
Rhegmatogenous RD
Pars planitis
Punctate outer retinitis
Serous macular detachment
BRAOBRVO
Retinal or subretinal neovascularization
Choroidoretinal vascular anastomosis
Panuveitis
Toxoplasmic retinitis ndash 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 rarr HEADLIGHT IN FOG
appearance
-In immunocompromised ndash multifocal retinal lesion often BL less vitritis - simulate ARN
- There may be sec nongranulomatous inflammation of choroid amp sclera
- When choroid is involved called as retinochoroiditis
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
3 Fungal
ndash Candidiasis
ndash Aspergillosis
ndash Cryptococcosis
ndash Coccidioidomycosis
NON-INFECTIOUS CAUSE
Multifocal Choroiditis
and Panuveitis
Punctate Inner
Choroidopathy
Subretinal Fibrosis
and Uveitis
Serpiginous
choroidopathy
Acute retinal pigment
epitheliitis
Birdshot
choroidopathy
1048698 Retinal Vasculitis
ndash Behcets
ndash SLE
ndash Wegeners
granulomatosis
ndash PAN
ndash Eales disease
ndash Frosted-branch
angiitis
SYMPTOMS
Floaters
Impaired central vision ( pain or painless )
Pain redness amp photophobia if associated
with ant Segment involvement
Metamorphopsia micromacropsia
Perception of black spot
SIGNS ndash
Inflammatory cells amp vitritis
Exudates Edema amp infiltrations in
retina choroid
Sheathing of vessels
Other signs ndash
Disc edema
Retinal haemorrhages
Spill-over uveitis
Complicated cataract
Glaucoma
RD
Choroid neovascularisation
CHOROIDITIS Focal multifocal diffusecentral juxtapapillary
Granulomatous or non-granulomatous exudative choroiditis
Ophthalmoscopic picture ndash
1 Active lesion ndash early stage - yellowish area with hazy edges amp ill defined margin due to infiltration amp exudation lie deeper to retinal vessels
- Late stage ndash bruchrsquos membrane destroyed ndash infiltration of leukocytes to retina amp vitreous
darr
organisation of exudation due to fibroblastic activity of stroma
darr
Firm fusion of retina amp choroid due to destruction of normal structure by fibrous tissue
Old choroiditis lesion ndash
- White colour lesion due to fibrous tissue deposition thinning amp atrophy ndash white reflex from sclera
Surrounded by black zone of pigment from RPE
RETINITIS - Focal multifocal geographic diffuse
Active lesions ndash whitis retinal opacities with indistinct boarder due to surronding edema
Later on boarder become well defined
VASCULITIS ndash Periphlebitis gt periarteritis
Active vasculitis ndash yellowishgrey-white patchy perivascular sheathing with haemorrhage
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 gt10 of adults in northern temperate
countries amp gt 50 of adults in
mediterranean amp tropical countries
Three forms of the parasite
- tachyzoite ( trophozoite) ndash invassive form responsible for acute infection
- bradyzoite ( tissue cyst) ndash latent or recurentinfection
- sporozoite (oocyst)
MODE OF INFECTION
Ingestion of undercooked meat containing bradyzoites
Ingestion of oocyst from contaminated hand food or water
Transplacental ndash 40 of fetus is affected if mother is infected during pregnancy
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 - uarred Plasma cells at periphery rarr secrete
antibodies rarr destruction of the free parasites in the
extracellular space rarr cyst formation by parasites
Proliferation of the RPE cells and healing of the
lesion is associated with scar formation
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 membranerarr a
group of protozoa surrounded by the retinal cell
membranerarr 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
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
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 ndash 1st trimester rarr spontaneous abortion
- 3rd trimester rarr subclinical infection
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
OCULAR MANIFESTATION
Ocular findings include involvement of the retina
choroid retinal vessels macula optic nerve
vitreous and anterior uvea
TYPICAL ndash
-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
Atypical Manifestations-Juxtapapillar retinitis
Retrobulbar neuritis
Rhegmatogenous RD
Pars planitis
Punctate outer retinitis
Serous macular detachment
BRAOBRVO
Retinal or subretinal neovascularization
Choroidoretinal vascular anastomosis
Panuveitis
Toxoplasmic retinitis ndash 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 rarr HEADLIGHT IN FOG
appearance
-In immunocompromised ndash multifocal retinal lesion often BL less vitritis - simulate ARN
- There may be sec nongranulomatous inflammation of choroid amp sclera
- When choroid is involved called as retinochoroiditis
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
NON-INFECTIOUS CAUSE
Multifocal Choroiditis
and Panuveitis
Punctate Inner
Choroidopathy
Subretinal Fibrosis
and Uveitis
Serpiginous
choroidopathy
Acute retinal pigment
epitheliitis
Birdshot
choroidopathy
1048698 Retinal Vasculitis
ndash Behcets
ndash SLE
ndash Wegeners
granulomatosis
ndash PAN
ndash Eales disease
ndash Frosted-branch
angiitis
SYMPTOMS
Floaters
Impaired central vision ( pain or painless )
Pain redness amp photophobia if associated
with ant Segment involvement
Metamorphopsia micromacropsia
Perception of black spot
SIGNS ndash
Inflammatory cells amp vitritis
Exudates Edema amp infiltrations in
retina choroid
Sheathing of vessels
Other signs ndash
Disc edema
Retinal haemorrhages
Spill-over uveitis
Complicated cataract
Glaucoma
RD
Choroid neovascularisation
CHOROIDITIS Focal multifocal diffusecentral juxtapapillary
Granulomatous or non-granulomatous exudative choroiditis
Ophthalmoscopic picture ndash
1 Active lesion ndash early stage - yellowish area with hazy edges amp ill defined margin due to infiltration amp exudation lie deeper to retinal vessels
- Late stage ndash bruchrsquos membrane destroyed ndash infiltration of leukocytes to retina amp vitreous
darr
organisation of exudation due to fibroblastic activity of stroma
darr
Firm fusion of retina amp choroid due to destruction of normal structure by fibrous tissue
Old choroiditis lesion ndash
- White colour lesion due to fibrous tissue deposition thinning amp atrophy ndash white reflex from sclera
Surrounded by black zone of pigment from RPE
RETINITIS - Focal multifocal geographic diffuse
Active lesions ndash whitis retinal opacities with indistinct boarder due to surronding edema
Later on boarder become well defined
VASCULITIS ndash Periphlebitis gt periarteritis
Active vasculitis ndash yellowishgrey-white patchy perivascular sheathing with haemorrhage
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 gt10 of adults in northern temperate
countries amp gt 50 of adults in
mediterranean amp tropical countries
Three forms of the parasite
- tachyzoite ( trophozoite) ndash invassive form responsible for acute infection
- bradyzoite ( tissue cyst) ndash latent or recurentinfection
- sporozoite (oocyst)
MODE OF INFECTION
Ingestion of undercooked meat containing bradyzoites
Ingestion of oocyst from contaminated hand food or water
Transplacental ndash 40 of fetus is affected if mother is infected during pregnancy
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 - uarred Plasma cells at periphery rarr secrete
antibodies rarr destruction of the free parasites in the
extracellular space rarr cyst formation by parasites
Proliferation of the RPE cells and healing of the
lesion is associated with scar formation
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 membranerarr a
group of protozoa surrounded by the retinal cell
membranerarr 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
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
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 ndash 1st trimester rarr spontaneous abortion
- 3rd trimester rarr subclinical infection
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
OCULAR MANIFESTATION
Ocular findings include involvement of the retina
choroid retinal vessels macula optic nerve
vitreous and anterior uvea
TYPICAL ndash
-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
Atypical Manifestations-Juxtapapillar retinitis
Retrobulbar neuritis
Rhegmatogenous RD
Pars planitis
Punctate outer retinitis
Serous macular detachment
BRAOBRVO
Retinal or subretinal neovascularization
Choroidoretinal vascular anastomosis
Panuveitis
Toxoplasmic retinitis ndash 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 rarr HEADLIGHT IN FOG
appearance
-In immunocompromised ndash multifocal retinal lesion often BL less vitritis - simulate ARN
- There may be sec nongranulomatous inflammation of choroid amp sclera
- When choroid is involved called as retinochoroiditis
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
SYMPTOMS
Floaters
Impaired central vision ( pain or painless )
Pain redness amp photophobia if associated
with ant Segment involvement
Metamorphopsia micromacropsia
Perception of black spot
SIGNS ndash
Inflammatory cells amp vitritis
Exudates Edema amp infiltrations in
retina choroid
Sheathing of vessels
Other signs ndash
Disc edema
Retinal haemorrhages
Spill-over uveitis
Complicated cataract
Glaucoma
RD
Choroid neovascularisation
CHOROIDITIS Focal multifocal diffusecentral juxtapapillary
Granulomatous or non-granulomatous exudative choroiditis
Ophthalmoscopic picture ndash
1 Active lesion ndash early stage - yellowish area with hazy edges amp ill defined margin due to infiltration amp exudation lie deeper to retinal vessels
- Late stage ndash bruchrsquos membrane destroyed ndash infiltration of leukocytes to retina amp vitreous
darr
organisation of exudation due to fibroblastic activity of stroma
darr
Firm fusion of retina amp choroid due to destruction of normal structure by fibrous tissue
Old choroiditis lesion ndash
- White colour lesion due to fibrous tissue deposition thinning amp atrophy ndash white reflex from sclera
Surrounded by black zone of pigment from RPE
RETINITIS - Focal multifocal geographic diffuse
Active lesions ndash whitis retinal opacities with indistinct boarder due to surronding edema
Later on boarder become well defined
VASCULITIS ndash Periphlebitis gt periarteritis
Active vasculitis ndash yellowishgrey-white patchy perivascular sheathing with haemorrhage
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 gt10 of adults in northern temperate
countries amp gt 50 of adults in
mediterranean amp tropical countries
Three forms of the parasite
- tachyzoite ( trophozoite) ndash invassive form responsible for acute infection
- bradyzoite ( tissue cyst) ndash latent or recurentinfection
- sporozoite (oocyst)
MODE OF INFECTION
Ingestion of undercooked meat containing bradyzoites
Ingestion of oocyst from contaminated hand food or water
Transplacental ndash 40 of fetus is affected if mother is infected during pregnancy
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 - uarred Plasma cells at periphery rarr secrete
antibodies rarr destruction of the free parasites in the
extracellular space rarr cyst formation by parasites
Proliferation of the RPE cells and healing of the
lesion is associated with scar formation
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 membranerarr a
group of protozoa surrounded by the retinal cell
membranerarr 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
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
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 ndash 1st trimester rarr spontaneous abortion
- 3rd trimester rarr subclinical infection
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
OCULAR MANIFESTATION
Ocular findings include involvement of the retina
choroid retinal vessels macula optic nerve
vitreous and anterior uvea
TYPICAL ndash
-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
Atypical Manifestations-Juxtapapillar retinitis
Retrobulbar neuritis
Rhegmatogenous RD
Pars planitis
Punctate outer retinitis
Serous macular detachment
BRAOBRVO
Retinal or subretinal neovascularization
Choroidoretinal vascular anastomosis
Panuveitis
Toxoplasmic retinitis ndash 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 rarr HEADLIGHT IN FOG
appearance
-In immunocompromised ndash multifocal retinal lesion often BL less vitritis - simulate ARN
- There may be sec nongranulomatous inflammation of choroid amp sclera
- When choroid is involved called as retinochoroiditis
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
SIGNS ndash
Inflammatory cells amp vitritis
Exudates Edema amp infiltrations in
retina choroid
Sheathing of vessels
Other signs ndash
Disc edema
Retinal haemorrhages
Spill-over uveitis
Complicated cataract
Glaucoma
RD
Choroid neovascularisation
CHOROIDITIS Focal multifocal diffusecentral juxtapapillary
Granulomatous or non-granulomatous exudative choroiditis
Ophthalmoscopic picture ndash
1 Active lesion ndash early stage - yellowish area with hazy edges amp ill defined margin due to infiltration amp exudation lie deeper to retinal vessels
- Late stage ndash bruchrsquos membrane destroyed ndash infiltration of leukocytes to retina amp vitreous
darr
organisation of exudation due to fibroblastic activity of stroma
darr
Firm fusion of retina amp choroid due to destruction of normal structure by fibrous tissue
Old choroiditis lesion ndash
- White colour lesion due to fibrous tissue deposition thinning amp atrophy ndash white reflex from sclera
Surrounded by black zone of pigment from RPE
RETINITIS - Focal multifocal geographic diffuse
Active lesions ndash whitis retinal opacities with indistinct boarder due to surronding edema
Later on boarder become well defined
VASCULITIS ndash Periphlebitis gt periarteritis
Active vasculitis ndash yellowishgrey-white patchy perivascular sheathing with haemorrhage
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 gt10 of adults in northern temperate
countries amp gt 50 of adults in
mediterranean amp tropical countries
Three forms of the parasite
- tachyzoite ( trophozoite) ndash invassive form responsible for acute infection
- bradyzoite ( tissue cyst) ndash latent or recurentinfection
- sporozoite (oocyst)
MODE OF INFECTION
Ingestion of undercooked meat containing bradyzoites
Ingestion of oocyst from contaminated hand food or water
Transplacental ndash 40 of fetus is affected if mother is infected during pregnancy
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 - uarred Plasma cells at periphery rarr secrete
antibodies rarr destruction of the free parasites in the
extracellular space rarr cyst formation by parasites
Proliferation of the RPE cells and healing of the
lesion is associated with scar formation
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 membranerarr a
group of protozoa surrounded by the retinal cell
membranerarr 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
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
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 ndash 1st trimester rarr spontaneous abortion
- 3rd trimester rarr subclinical infection
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
OCULAR MANIFESTATION
Ocular findings include involvement of the retina
choroid retinal vessels macula optic nerve
vitreous and anterior uvea
TYPICAL ndash
-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
Atypical Manifestations-Juxtapapillar retinitis
Retrobulbar neuritis
Rhegmatogenous RD
Pars planitis
Punctate outer retinitis
Serous macular detachment
BRAOBRVO
Retinal or subretinal neovascularization
Choroidoretinal vascular anastomosis
Panuveitis
Toxoplasmic retinitis ndash 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 rarr HEADLIGHT IN FOG
appearance
-In immunocompromised ndash multifocal retinal lesion often BL less vitritis - simulate ARN
- There may be sec nongranulomatous inflammation of choroid amp sclera
- When choroid is involved called as retinochoroiditis
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
CHOROIDITIS Focal multifocal diffusecentral juxtapapillary
Granulomatous or non-granulomatous exudative choroiditis
Ophthalmoscopic picture ndash
1 Active lesion ndash early stage - yellowish area with hazy edges amp ill defined margin due to infiltration amp exudation lie deeper to retinal vessels
- Late stage ndash bruchrsquos membrane destroyed ndash infiltration of leukocytes to retina amp vitreous
darr
organisation of exudation due to fibroblastic activity of stroma
darr
Firm fusion of retina amp choroid due to destruction of normal structure by fibrous tissue
Old choroiditis lesion ndash
- White colour lesion due to fibrous tissue deposition thinning amp atrophy ndash white reflex from sclera
Surrounded by black zone of pigment from RPE
RETINITIS - Focal multifocal geographic diffuse
Active lesions ndash whitis retinal opacities with indistinct boarder due to surronding edema
Later on boarder become well defined
VASCULITIS ndash Periphlebitis gt periarteritis
Active vasculitis ndash yellowishgrey-white patchy perivascular sheathing with haemorrhage
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 gt10 of adults in northern temperate
countries amp gt 50 of adults in
mediterranean amp tropical countries
Three forms of the parasite
- tachyzoite ( trophozoite) ndash invassive form responsible for acute infection
- bradyzoite ( tissue cyst) ndash latent or recurentinfection
- sporozoite (oocyst)
MODE OF INFECTION
Ingestion of undercooked meat containing bradyzoites
Ingestion of oocyst from contaminated hand food or water
Transplacental ndash 40 of fetus is affected if mother is infected during pregnancy
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 - uarred Plasma cells at periphery rarr secrete
antibodies rarr destruction of the free parasites in the
extracellular space rarr cyst formation by parasites
Proliferation of the RPE cells and healing of the
lesion is associated with scar formation
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 membranerarr a
group of protozoa surrounded by the retinal cell
membranerarr 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
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
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 ndash 1st trimester rarr spontaneous abortion
- 3rd trimester rarr subclinical infection
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
OCULAR MANIFESTATION
Ocular findings include involvement of the retina
choroid retinal vessels macula optic nerve
vitreous and anterior uvea
TYPICAL ndash
-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
Atypical Manifestations-Juxtapapillar retinitis
Retrobulbar neuritis
Rhegmatogenous RD
Pars planitis
Punctate outer retinitis
Serous macular detachment
BRAOBRVO
Retinal or subretinal neovascularization
Choroidoretinal vascular anastomosis
Panuveitis
Toxoplasmic retinitis ndash 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 rarr HEADLIGHT IN FOG
appearance
-In immunocompromised ndash multifocal retinal lesion often BL less vitritis - simulate ARN
- There may be sec nongranulomatous inflammation of choroid amp sclera
- When choroid is involved called as retinochoroiditis
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
Old choroiditis lesion ndash
- White colour lesion due to fibrous tissue deposition thinning amp atrophy ndash white reflex from sclera
Surrounded by black zone of pigment from RPE
RETINITIS - Focal multifocal geographic diffuse
Active lesions ndash whitis retinal opacities with indistinct boarder due to surronding edema
Later on boarder become well defined
VASCULITIS ndash Periphlebitis gt periarteritis
Active vasculitis ndash yellowishgrey-white patchy perivascular sheathing with haemorrhage
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 gt10 of adults in northern temperate
countries amp gt 50 of adults in
mediterranean amp tropical countries
Three forms of the parasite
- tachyzoite ( trophozoite) ndash invassive form responsible for acute infection
- bradyzoite ( tissue cyst) ndash latent or recurentinfection
- sporozoite (oocyst)
MODE OF INFECTION
Ingestion of undercooked meat containing bradyzoites
Ingestion of oocyst from contaminated hand food or water
Transplacental ndash 40 of fetus is affected if mother is infected during pregnancy
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 - uarred Plasma cells at periphery rarr secrete
antibodies rarr destruction of the free parasites in the
extracellular space rarr cyst formation by parasites
Proliferation of the RPE cells and healing of the
lesion is associated with scar formation
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 membranerarr a
group of protozoa surrounded by the retinal cell
membranerarr 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
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
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 ndash 1st trimester rarr spontaneous abortion
- 3rd trimester rarr subclinical infection
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
OCULAR MANIFESTATION
Ocular findings include involvement of the retina
choroid retinal vessels macula optic nerve
vitreous and anterior uvea
TYPICAL ndash
-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
Atypical Manifestations-Juxtapapillar retinitis
Retrobulbar neuritis
Rhegmatogenous RD
Pars planitis
Punctate outer retinitis
Serous macular detachment
BRAOBRVO
Retinal or subretinal neovascularization
Choroidoretinal vascular anastomosis
Panuveitis
Toxoplasmic retinitis ndash 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 rarr HEADLIGHT IN FOG
appearance
-In immunocompromised ndash multifocal retinal lesion often BL less vitritis - simulate ARN
- There may be sec nongranulomatous inflammation of choroid amp sclera
- When choroid is involved called as retinochoroiditis
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
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 gt10 of adults in northern temperate
countries amp gt 50 of adults in
mediterranean amp tropical countries
Three forms of the parasite
- tachyzoite ( trophozoite) ndash invassive form responsible for acute infection
- bradyzoite ( tissue cyst) ndash latent or recurentinfection
- sporozoite (oocyst)
MODE OF INFECTION
Ingestion of undercooked meat containing bradyzoites
Ingestion of oocyst from contaminated hand food or water
Transplacental ndash 40 of fetus is affected if mother is infected during pregnancy
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 - uarred Plasma cells at periphery rarr secrete
antibodies rarr destruction of the free parasites in the
extracellular space rarr cyst formation by parasites
Proliferation of the RPE cells and healing of the
lesion is associated with scar formation
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 membranerarr a
group of protozoa surrounded by the retinal cell
membranerarr 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
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
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 ndash 1st trimester rarr spontaneous abortion
- 3rd trimester rarr subclinical infection
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
OCULAR MANIFESTATION
Ocular findings include involvement of the retina
choroid retinal vessels macula optic nerve
vitreous and anterior uvea
TYPICAL ndash
-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
Atypical Manifestations-Juxtapapillar retinitis
Retrobulbar neuritis
Rhegmatogenous RD
Pars planitis
Punctate outer retinitis
Serous macular detachment
BRAOBRVO
Retinal or subretinal neovascularization
Choroidoretinal vascular anastomosis
Panuveitis
Toxoplasmic retinitis ndash 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 rarr HEADLIGHT IN FOG
appearance
-In immunocompromised ndash multifocal retinal lesion often BL less vitritis - simulate ARN
- There may be sec nongranulomatous inflammation of choroid amp sclera
- When choroid is involved called as retinochoroiditis
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
Three forms of the parasite
- tachyzoite ( trophozoite) ndash invassive form responsible for acute infection
- bradyzoite ( tissue cyst) ndash latent or recurentinfection
- sporozoite (oocyst)
MODE OF INFECTION
Ingestion of undercooked meat containing bradyzoites
Ingestion of oocyst from contaminated hand food or water
Transplacental ndash 40 of fetus is affected if mother is infected during pregnancy
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 - uarred Plasma cells at periphery rarr secrete
antibodies rarr destruction of the free parasites in the
extracellular space rarr cyst formation by parasites
Proliferation of the RPE cells and healing of the
lesion is associated with scar formation
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 membranerarr a
group of protozoa surrounded by the retinal cell
membranerarr 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
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
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 ndash 1st trimester rarr spontaneous abortion
- 3rd trimester rarr subclinical infection
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
OCULAR MANIFESTATION
Ocular findings include involvement of the retina
choroid retinal vessels macula optic nerve
vitreous and anterior uvea
TYPICAL ndash
-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
Atypical Manifestations-Juxtapapillar retinitis
Retrobulbar neuritis
Rhegmatogenous RD
Pars planitis
Punctate outer retinitis
Serous macular detachment
BRAOBRVO
Retinal or subretinal neovascularization
Choroidoretinal vascular anastomosis
Panuveitis
Toxoplasmic retinitis ndash 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 rarr HEADLIGHT IN FOG
appearance
-In immunocompromised ndash multifocal retinal lesion often BL less vitritis - simulate ARN
- There may be sec nongranulomatous inflammation of choroid amp sclera
- When choroid is involved called as retinochoroiditis
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
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 - uarred Plasma cells at periphery rarr secrete
antibodies rarr destruction of the free parasites in the
extracellular space rarr cyst formation by parasites
Proliferation of the RPE cells and healing of the
lesion is associated with scar formation
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 membranerarr a
group of protozoa surrounded by the retinal cell
membranerarr 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
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
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 ndash 1st trimester rarr spontaneous abortion
- 3rd trimester rarr subclinical infection
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
OCULAR MANIFESTATION
Ocular findings include involvement of the retina
choroid retinal vessels macula optic nerve
vitreous and anterior uvea
TYPICAL ndash
-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
Atypical Manifestations-Juxtapapillar retinitis
Retrobulbar neuritis
Rhegmatogenous RD
Pars planitis
Punctate outer retinitis
Serous macular detachment
BRAOBRVO
Retinal or subretinal neovascularization
Choroidoretinal vascular anastomosis
Panuveitis
Toxoplasmic retinitis ndash 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 rarr HEADLIGHT IN FOG
appearance
-In immunocompromised ndash multifocal retinal lesion often BL less vitritis - simulate ARN
- There may be sec nongranulomatous inflammation of choroid amp sclera
- When choroid is involved called as retinochoroiditis
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
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 membranerarr a
group of protozoa surrounded by the retinal cell
membranerarr 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
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
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 ndash 1st trimester rarr spontaneous abortion
- 3rd trimester rarr subclinical infection
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
OCULAR MANIFESTATION
Ocular findings include involvement of the retina
choroid retinal vessels macula optic nerve
vitreous and anterior uvea
TYPICAL ndash
-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
Atypical Manifestations-Juxtapapillar retinitis
Retrobulbar neuritis
Rhegmatogenous RD
Pars planitis
Punctate outer retinitis
Serous macular detachment
BRAOBRVO
Retinal or subretinal neovascularization
Choroidoretinal vascular anastomosis
Panuveitis
Toxoplasmic retinitis ndash 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 rarr HEADLIGHT IN FOG
appearance
-In immunocompromised ndash multifocal retinal lesion often BL less vitritis - simulate ARN
- There may be sec nongranulomatous inflammation of choroid amp sclera
- When choroid is involved called as retinochoroiditis
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
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
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 ndash 1st trimester rarr spontaneous abortion
- 3rd trimester rarr subclinical infection
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
OCULAR MANIFESTATION
Ocular findings include involvement of the retina
choroid retinal vessels macula optic nerve
vitreous and anterior uvea
TYPICAL ndash
-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
Atypical Manifestations-Juxtapapillar retinitis
Retrobulbar neuritis
Rhegmatogenous RD
Pars planitis
Punctate outer retinitis
Serous macular detachment
BRAOBRVO
Retinal or subretinal neovascularization
Choroidoretinal vascular anastomosis
Panuveitis
Toxoplasmic retinitis ndash 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 rarr HEADLIGHT IN FOG
appearance
-In immunocompromised ndash multifocal retinal lesion often BL less vitritis - simulate ARN
- There may be sec nongranulomatous inflammation of choroid amp sclera
- When choroid is involved called as retinochoroiditis
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
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 ndash 1st trimester rarr spontaneous abortion
- 3rd trimester rarr subclinical infection
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
OCULAR MANIFESTATION
Ocular findings include involvement of the retina
choroid retinal vessels macula optic nerve
vitreous and anterior uvea
TYPICAL ndash
-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
Atypical Manifestations-Juxtapapillar retinitis
Retrobulbar neuritis
Rhegmatogenous RD
Pars planitis
Punctate outer retinitis
Serous macular detachment
BRAOBRVO
Retinal or subretinal neovascularization
Choroidoretinal vascular anastomosis
Panuveitis
Toxoplasmic retinitis ndash 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 rarr HEADLIGHT IN FOG
appearance
-In immunocompromised ndash multifocal retinal lesion often BL less vitritis - simulate ARN
- There may be sec nongranulomatous inflammation of choroid amp sclera
- When choroid is involved called as retinochoroiditis
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
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
OCULAR MANIFESTATION
Ocular findings include involvement of the retina
choroid retinal vessels macula optic nerve
vitreous and anterior uvea
TYPICAL ndash
-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
Atypical Manifestations-Juxtapapillar retinitis
Retrobulbar neuritis
Rhegmatogenous RD
Pars planitis
Punctate outer retinitis
Serous macular detachment
BRAOBRVO
Retinal or subretinal neovascularization
Choroidoretinal vascular anastomosis
Panuveitis
Toxoplasmic retinitis ndash 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 rarr HEADLIGHT IN FOG
appearance
-In immunocompromised ndash multifocal retinal lesion often BL less vitritis - simulate ARN
- There may be sec nongranulomatous inflammation of choroid amp sclera
- When choroid is involved called as retinochoroiditis
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
OCULAR MANIFESTATION
Ocular findings include involvement of the retina
choroid retinal vessels macula optic nerve
vitreous and anterior uvea
TYPICAL ndash
-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
Atypical Manifestations-Juxtapapillar retinitis
Retrobulbar neuritis
Rhegmatogenous RD
Pars planitis
Punctate outer retinitis
Serous macular detachment
BRAOBRVO
Retinal or subretinal neovascularization
Choroidoretinal vascular anastomosis
Panuveitis
Toxoplasmic retinitis ndash 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 rarr HEADLIGHT IN FOG
appearance
-In immunocompromised ndash multifocal retinal lesion often BL less vitritis - simulate ARN
- There may be sec nongranulomatous inflammation of choroid amp sclera
- When choroid is involved called as retinochoroiditis
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
Atypical Manifestations-Juxtapapillar retinitis
Retrobulbar neuritis
Rhegmatogenous RD
Pars planitis
Punctate outer retinitis
Serous macular detachment
BRAOBRVO
Retinal or subretinal neovascularization
Choroidoretinal vascular anastomosis
Panuveitis
Toxoplasmic retinitis ndash 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 rarr HEADLIGHT IN FOG
appearance
-In immunocompromised ndash multifocal retinal lesion often BL less vitritis - simulate ARN
- There may be sec nongranulomatous inflammation of choroid amp sclera
- When choroid is involved called as retinochoroiditis
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
Toxoplasmic retinitis ndash 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 rarr HEADLIGHT IN FOG
appearance
-In immunocompromised ndash multifocal retinal lesion often BL less vitritis - simulate ARN
- There may be sec nongranulomatous inflammation of choroid amp sclera
- When choroid is involved called as retinochoroiditis
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
Occurs in 3 morphological variants -
1 In most severe disease ndash lesion of gt 1 DD dense amp elevated lesion amp are largely destructive
- assosiated with severe vitritis amp 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
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
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
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
COMPLICATIONS Posterior synaechiae
Macular edema
Dragging of macula
RD
Choroidal neovascularisation
BRAOBRVO
Optic atrophy
Cataract
Glaucoma
ul pigmentary retinopathy
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
DIAGNOSIS Classic fundus finding
Serological testing ndash
- 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
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
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 grday in two divided doses
Standard regimen for newborns- Pyrimethamine + Sulfadiazine + Folinicacid
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
SURGICAL Tt ndash
- 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
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
TOXOCARIASIS
Toxocara canis nematode
Dog primary host
Children who have pica close contact with Puppies
Unilateral Male gt female Children young adults
DDx of leukocoria (ro RB)
1048698 Ova ingested
ndash Visceral larva migrans
ndash Larvae encyst in tissues
ndash Never mature in humans ndash no ova in stool
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
CLINICAL FEATURES
1 Granuloma in the Peripheral Retina and
Vitreous
2 Posterior Pole Granuloma
3 Chronic Endophthalmitis
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
DIAGNOSIS Anti-Toxocara antibodies
ndash Any serum titer significant
ndash Higher titer in aqueous
Eosinophils in aqueousvitreous
TREATMENTMedical 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
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
Cysticercosis- SouthCentral America Africa Asia
- Larva of Taenia solium
- Violent uveitis as endophthalmitis
Treatment vitrectomy for subretinal cysticercus
Onchocerciasis River blindnessrdquo - blackflies
Microfilariae in cornea aqueous skin nodules
Attenuated vessels perivascular sheathing RPE atrophy optic atrophy late
Ivermectin 150 mickg q year x 10 years
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
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 choroiditiswhich 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 bl
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
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
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
Rubella
Congenital
ndash Ocular involvement increased if contracted during 1st trimester
ndash Cataract - retention of cell nuclei in embryonic nucleus
ndash Chronic nongranulomatous iritis iris atrophy
- ldquoSalt-and-pepperrdquo fundus ndash vision ERG unaffected
ndash Choroidal neovascularization rare complication
Acquired
ndash German measles
ndash Conjunctivitis keratitis iritis bilateral retinitis with exudative detachment
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
Measles (Rubeola)
1048698 Congenital
ndash ldquoSalt-and-pepperrdquo fundus
1048698 Acquired
ndash Macular edema neuroretinitis attenuated vessels
1048698 Subacute sclerosing panencephalitis (SSPE)
ndash Slow virus - mutation of measles virus
ndash Encephalitis with progressive deficits
ndash Disc edema optic atrophy macular
- infiltratehemorrhagegliosis
ndash Supportive treatment poor prognosis
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
West Nile Virus
Creamy target like chorioretinal lesions 300 ndash 1000
μm scattered diffusely
Hypofluorescent centrally and hyperfluorescent
edges
Multifocal chorioretinitis
ndash Vitritis iridocyclitis
ndash Occlusive retinal vasculitis - multiple branch artery
occlusions
ndash Optic nerve optic neuritis mild disc edema
1048698 Congenital - chorioretinal scarring
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
FUNGAL UVEITIS
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
Ocular Histoplasmosis presumed
occular histoplasmosis syndrome
Histoplasma capsulatum
20 ndash 50 yr HLA-B7 ndash associated with macular lesions
Punched-out CR scars (ldquohisto spotsrdquo)
Peripapillary atrophy Macular scar No vitreous cells
FA -
ndash Active choroiditis early hypofluorescence with late staining
ndash CNV early hyperfluorescence with late leakage
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
Treatment -
ndash Extrafoveal CNV photocoagulation
- Juxtafoveal CNV photocoagulation
ndash Risk of CNV in fellow eye with histo spot in
macula 25 3 years
SF CNV-
Photodynamic therapy SteroidsAnti-VEGF
Combination
Subfoveal surgery- benefit for POHS if lt 20100
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
Candidiasis
Immunosuppressed patients indwelling catheters hyperalimentation
Incidence of endophthalmitis in candidemia
ndash No antifungal treatment ndash 10 ndash 37
ndash On antifungal treatment ndash 3
Choroidal infection with secondary retinal
vitreous involvement ndash fluffy yellow lesions
Treatment
ndash IV periocular intravitreal antifungals (amphotericin B ketoconazole)
ndash Consider vitrectomy if significant vitritis
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
NON INFECTIOUS CAUSE
MULTIFOCAL CHOROIDITIS amp PANUVEITIS (
MCP )
1048698 Female gt male
1048698 ldquoPseudo-POHSrdquo ndash histo spots
1048698 Vitritis +- anterior uveitis
1048698 Macular CNV in 13
1048698 FA Early hyperfluorescence with late staining
1048698 Diagnosis of exclusion- TB syphilis sarcoidosis
1048698 Treatment
ndash Steroids ndash Local Systemic
ndash Other immunosuppressives
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
Punctate Inner Choroidopathy (PIC)- Subgroup of MCP
- Young female myopic
- No inflammation
- Multiple small white spots with fuzzy boarder at
Inner choroid amp 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)
ndash other immunosuppressives
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
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
ndash Early in disease ndash like AMPPE
ndash Later in disease ndash window defects
Steroids other immunosuppressives
Poor prognosis
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
Birdshot Retinochoroidopathy (BSRC)
Vitiliginous choroiditis
Females gt males 30 ndash 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
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
FA
ndash Retinal lesions often silent
ndash CME periphlebitis
Diagnostic
ndash HLA-A29 - 50-80 birdshot
ERG may be reduced
Treatment
ndash Corticosteroids ndash may help in ~ 50
ndash immunosuppressives - Mycophenolate Cyclosporine
bull Quiescent 2 yrs then slow taper
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
THANK YOU
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
THANK YOU
THANK YOU
