Uvea

Dr. Renu Thakur Ph.D.

 Anatomy of Uvea
• Uvea is the vascular coat of eye ball and lies
between the sclera and retina.

• Uvea is composed of three parts i.e. iris, ciliary

body and choroid
Uvea
IRIS
Anterior surface has two zones:

1) Papillary zone: is flat and has a dark border at

the papillary margin , known as papillary ruff.
Junction of papillary and ciliary zone is marked
by a smooth ridge known as collaret.

2) Ciliary zone: towards the ciliary border has ciliary

crypts. Histologically iris has got 5 layers (from
before backward).

1- Endothelium: flat nucleated cells absent over the

crypts probably to allow free movement of the
aqueous in and out of the iris.
2- Vessel layer: consist of blood vessels lying in collagen
fibers, chromotophores etc.,

3- Muscular layer: two muscles:

a) Sphincter pupillae- plain muscle developed from

neuroectoderm- supplied by parasympathetic fibers
coming through the 3rd nerve (relayed in ciliary
ganglion).

b) Dilator pupillae- also arise from neuroectoderm and

supplied by cervical sympathetic fibers reaching the eye
through long ciliary nerves (not relayed in ciliary
ganglion).
4- Pigmented epithelium- two layers.

The two layers are loosely attached to each other and

there is a potential space between the 2 layers.
5- Internal limiting membrane- fine and homogenous
structure, not consistently present.

Function of the iris:

1- Regulates the entry of light into the eye by changing

the size of papillary aperture.

2- Cuts away the peripheral aberrations.

3-Absorption of aqueous also takes place from its

surface.
2) Ciliary body:

Ciliary body is a ring shaped structure placed more

or less sagitally and extends from the ora-serrata to
the scleral spur.

It consists of ciliary processes and ciliary muscle. On

longitudinal section it is triangular. It’s anterior
surface or base is shortest. Iris is attached to the base.

The outer side of triangle is adjacent to sclera and is

formed by ciliary muscle.
Ciliary body
Ciliary body
The inner surface is directed towards the cavity of
the eye ball and is divided into two portions anterior
(pars plicata ) and posterior (pars plana).

Ciliary muscle consists of:

1. Meridional fibers.

2. Circular fibers.

3. Radiating fibers.
Meridional fibers on contraction pull the suprachoroidea
forwards and release the suspensory ligament allowing
the lens to become more convex as in accommodation.

The pars plicata has about 70 ciliary processes.They

secrete aqueous.
Functions of ciliary body:

1. Brings about accommodation.

2. Formation of aqueous.

3. Helps in drainage of aqueous at the angle of anterior

chamber.
3) Choroid:

Choroid is the analogue of pia-arachnoid of the brain

and serves the same purpose of supplying nutrition to
the neural portion of eye i.e. retina. Choroid is
composed of five portions.

1. The outer most is SUPRACHOROIDEA a potential

space between the choroid and sclera. This is lined by
endothelium and traversed by fibrous trabeculae.
This space is utilized for the treatment of aphakic
glaucoma in the operation of cyclodialysis.
Deeper to it are three vascular layers.

2. Layer of LARGE BLOOD VESSELS is outer most.

3. Next comes MEDIUM SIZED BLOOD VESSELES.

4. and SMALL BLOOD VESSELES or CHOROIDO-

CAPILLARIES.
Layer of choriocapillaries is the most important. It
serves to provide nutrition to the outer layers of
retina. The choriocapillaries are much wider than the
capillaries elsewhere.
Their diameter varies from 10 to 30 microns.

5. The innermost layer is avascular known as

MEMBRANE of BRUCHS. This is composed of
elastic and cuticular lamina and pigment epithelium
of retina is intimately attached to it.
 Classification
• Anatomical Classification

• Clinical Classification

• Etiological Classification

• Pathological Classification
 Anatomical Classification
• 1) Anterior Uveitis – Inflammation of iris and
anterior part of ciliary body.

• 2) Intermediate Uveitis – Involvement of posterior

part of ciliary body and extreme periphery of
retina. (Pars planitis)

• 3) Posterior uveitis – Retinochoroiditis, choroiditis,

retinitis, chorioretinitis

• 4) Diffuse or pan uveitis – Involvement of entire

uveal tract
 Clinical Classification
1) Acute – sudden symptomatic onset. Persists for 6 weeks or
less.
2) Chronic – Frequently insidious and asymptomatic. Persists for
months or years
 Etiological Classification
One of the most difficult problems in ophthalmology.
In most of the cases, probably, allergy is the cause.

1) Exogenous- introduction of organism into the eye through

a perforating wound or ulcer. acute iridocyclitis of
suppurative type, pan-ophthalmitis.

2) Secondary infection- Due to direct spread from adjoining

structures-
Cornea
Sclera
Retina
 Etiological Classification
3) Endogenous
Bacterial e.g. TB, Syphilis, gonorrhea
Viral e.g. Mumps, Small pox, influenza
Protozoal e.g. toxoplasmosis

4) Allergic inflammation
Result of an antigen-antibody reaction occurring in the eye due
to previous sensitization of uveal tissue to some allergen.

The allergen is a foreign protein. Most of the cases of

iridocyclitis do not have any specific cause and are probably
allergic in nature
5)Auto-immune/Constitutional-

a)Immune disorders affecting the body as a whole have ocular

manifestations in the form of iridocyclitis.
e.g. rheumatoid arthritis, SLE (Systemic Lupus Erythematosus),
ankylosing spondylitis, Reiter’s syndrome, Behcet’s Syndrome.

b) response to antigenic stimuli in other part of the eye.

Iridocyclitis is a common accompaniment of severe corneal
infection and choroiditis of retinal inflammation.
HLA (human leukocyte antigen)antigenic involvement
Disproportionately high percentage of patients of B-27 antigenic
group develop acute anterior uveitis.
Pathological Classification
 PATHOLOGY AND CLINICAL SIGNS-
Inflammation of iris and ciliary body

Dilatation of blood vessels

Iris stromal edema.

SIGNS - Iris pattern altered.Iris colour altered. Iris

thickened. Also accompanied by, ciliary congestion,
conjunctival hyperaemia and chemosis of
conjunctiva.
 Exudation of fibrin-rich fluid and inflammatory
cells in the tissues

Exudates escape into anterior chamber

Plasmoid aqueous
• SIGNS - Aqueous flare (like the beam of projector in
smokey theatre)
Nutrition of corneal endothelium is
affected due to toxins

Corneal endothelium becomes sticky

and edematous

Cells desquamated at places

Inflammatory cells stick to endothelial layer
as cellular deposits .

SIGN – Keratic precipitates

 In very intense cases, polymorphs pour out to
sink to bottom of anterior chamber
SIGN – Hypopyon
 Exudates cover the iris as a thin film and spread over
pupillary area
SIGN – Irritation of iris musculature constrictor being
more powerful than dilator, spasm results in miosis.

If exudate is profuse
SIGN – Plastic iritis

Blockage of pupil
SIGN – impairment of sight.
 In early stages, there is adhesion of iris to lens capsule
(Atropine may free the iris)

SIGN – Spots of exudate or pigment derived from posterior layer of iris

left permanently upon anterior capsule of lens (valuable evidence of
previous iritis)

Later on, the organization of the adhesion leads to formation of fibrous

bands between pupillary margin of iris and lens capsule (atropine
cannot rupture them)
SIGN – Posterior synechiae (more in lower part of pupil due to effect of
gravity)
 When adhesions are localized and a
mydriatic is instilled, it causes intervening
portions of circle of pupil to dilate.

SIGN– Festooned pupil (due

to irregular dilatation and is a
sign of present or past iritis.)
 Pigment epithelium on posterior surface is
pulled around pupillary margin so that patches
of pigment on anterior surface of iris are seen.

SIGN – Ectropion of uveal pigment (due to

contraction of organizing exudates upon iris)

With recurrent attacks or severe cases, the

whole circle of pupillary margin gets tied to lens
capsule.

SIGNS – Annular or ring synechiae or Seclusio

pupillae
Collection of aqueous behind iris since aqueous
drainage is hampered.

Iris is hence bowed forwards like sail.

SIGN – Iris Bombe (anterior chamber is funnel

shaped i.e. deepest in centre, shallowest at
periphery)
As iris bulges forward and comes into contact with cornea

Adhesions of iris to cornea at periphery develop

SIGNS – Peripheral anterior synechiae

Obliteration of filtration angle (Hypertensive iridocyclitis)

SIGNS – Rise in IOT (secondary glaucoma)
 When exudate is more extensive

Organization of exudate across entire pupillary area

Film of opaque fibrous tissue in pupillary area

SIGNS – Occlusio pupillae or Blocked pupil
Exudates fill up posterior chamber if there is much of cyclitis

When these adhesions organize, the iris adheres to lens

capsule.
SIGNS – Total posterior synechiae
When these adhesions organize, the iris
adheres to lens capsule.
SIGNS – Total posterior synechiae

Retraction of peripheral part of iris

Anterior chamber is abnormally deep at

periphery

In worst cases of plastic iridocyclitis

Cyclitic membrane formed
behind lens

Finally, degenerative
changes in ciliary body

Vitreous becomes fluid

Nutrition of lens impaired

SIGNS – Complicated
cataract
 In final stages, there is
interference with
secretion of aqueous

Fall in IOT

Eye shrinks (development of

soft eye is an ominous
sign)
SIGNS – Phthisis bulbi
 Clinical Features
SYMPTOMS SIGNS

• Pain • Signs of vascular

• Diminished vision congestion
• Redness of eye • Signs of exudation
• lacrimation • Signs of pupillary
• photophobia changes
• haloes around light
Uveitis associated
with arthritis
Uveitis associated with arthritis

• Ankylosing spondylitis
• Reiter’s syndrome
• Psoriatic arthritis
• Juvenile chronic arthritis
 Ankylosing spondylitis

• Acute iritis, Sacroiliitis and spondylitis

• IgM negative

• HLA-B27

• HLA-B27 is a blood test to look for a protein that is found on the

surface of white blood cells. The protein is called human leukocyte
antigen B27 (HLA-B27).

• Human leukocyte antigens (HLAs) are proteins that help the body's
immune system tell the difference between its own cells and
foreign, harmful substances
Ankylosing spondylitis prevalence
• General population: 5%
• Acute iritis: 45%
• AS: 90%
• Both AS & acute iritis: 95%
 Ocular features With Ankylosing
spondylitis
• Acute
• Recurrent
• Non granulomatous iritis

• Vision threatening complication are rear

• In few patients recurrent attack can become
chronic
 Reiter Syndrome
• Young adult male
• Classic triad
• Urethritis
• Polyarthritis
• Conjunctivitis (the most common) or acute
iritis
Ocular features With Reiter Syndrome
• Conjunctivitis
• Acute iritis
• Kerititis
Psoriatic arthritis
Psoriatic arthritis
 Psoriatic arthritis
• Psoriasis
• Psoriasis is a chronic skin condition caused by
an overactive immune system.
• Symptoms include flaking, inflammation, and
thick, white, silvery, or red patches of skin.
• Psoriasis treatments include steroid creams,
occlusion, light therapy and oral medications
Ocular features With Psoriatic arthritis

• Conjunctivitis
• Acute iritis
• Keratitis
• Secondary sjogrens syndrome
Juvenile chronic arthritis
 Systemic onset JIA
• Affects about 10 percent of children with arthritis.

• It begins with repeating fevers that can be 103°F or higher, often

accompanied by a salmon-colored rash that comes and goes.

• Systemic onset JIA may cause inflammation of the internal organs as

well as the joints, though joint swelling may not appear until
months or even years after the fevers begin.

• Anemia (a low red blood cell count) and elevated white blood cell
counts are also typical findings in blood tests ordered to evaluate
the fevers and ongoing symptoms. Arthritis may persist even after
the fevers and other symptoms have disappeared.
 Oligoarticular JIA
• Affects about half of all children with arthritis. Girls are
more at risk than boys.

• Older children with oligoarticular JIA may develop

“extended” arthritis that involves multiple joints and lasts
into adulthood.

• Children who develop the oligoarticular form of JIA when

they are younger than 7 years old have the best chance of
having their joint disease subside with time.

• They are, however, at increased risk of developing an

inflammatory eye problem (iritis or uveitis).
 Polyarticular JIA
• Affects five or more joints and can begin at
any age.
• Children diagnosed with polyarticular JIA in
their teens may actually have the adult form
of rheumatoid arthritis at an earlier-than-
usual age.
Ocular features With Juvenile chronic
arthritis
Ocular features With Juvenile chronic
arthritis
Ocular features With Juvenile chronic
arthritis
Uveitis in non infectious
Systemic disease
Uveitis in non infectious Systemic disease

• Sarcoidosis
• Behcet’s Disease
• Vogt-Koyanagi-Harada syndrome
 Sarcoidosis

• Sarcoidosis is a multisystem inflammatory

disease of unknown etiology that manifests as
noncaseating granulomas, predominantly in
the lungs and intrathoracic lymph nodes
 Sarcoidosis

• Asymptomatic (incidentally detected on chest imaging):

Approximately 5% of cases

• Systemic complaints (fever, anorexia): 45% of cases

• Pulmonary complaints (dyspnea on exertion, cough, chest

pain, and hemoptysis [rare]): 50% of cases

• Löfgren syndrome (fever, bilateral hilar lymphadenopathy,

and polyarthralgias): Common in Scandinavian patients, but
uncommon in African-American and Japanese patients
 Sarcoidosis
• Aetiology?
Genetic susceptibility – environmental provocateur
• Possible associated micro-organisms:
– Cell wall-deficient mycobacteria - MAC, M. paratuberculosis
– Propionibacteria - P.acnes, P.granulosum
– Chlamydia trachomatis
– Human herpesvirus Type 8
– Rickettsia helvetica
• Seasonal peaks of presentation
• Significant exposure to:
– Titanium
– Dust in vegetable processing
– Sustained high humidity
– Photocopier tone
 Ocular features With Sarcoidosis
• Characteristically a “granulomatous” uveitis:
• Large inferior KPs
• Greasy, mutton-fat
• Partly confluent
• Often glueing angle
– Presentation subacute
– Eye relatively white
– Raised IOP frequent
– PS/PAS frequent
Ocular features With Sarcoidosis
 Ocular features With Sarcoidosis

• Iris nodules are infrequent

• –Typically irregular in distribution
• –Typically smallish, sticky
• –Rarely large:
• –If so, sometimes vascularised
 The vitreous in sarcoidosis
• 15% of sarcoid uveitis presents as intermediate-
type, with large-ish opacities, inferior snowballs
+/- snowbanking
•10% of intermediates diagnosed sarcoidosis
 Retinal vasculature
• Intermittent periphlebitis with:
•exudate
•tortuosity
•narrowing
 Retinal vasculature
• Macroaneurysm
 Choroid and retina
• Typical - multifocal choroiditis
• –Smallish, creamy, moderately-well defined
• –Especially in inferior and nasal fundus, but
may be widespread
 Choroid and retina
• Multifocal choroiditis scars
• –Punctate, peripheral, inferior hemisphere
• •Peripheral multifocal chorioretinitis
• –Sometimes associated with sarcoidosis
Very uncommon – solitary nodule
Optic nerve head
 BEHÇET’S DISEASE
• Idiopathic multisystem
disease
• More common in men
• Occurs in 3rd - 4th decade
• Highest incidence in
Mediterranean region
and Japan
• Associated with HLA-B5

83
 BEHÇET’S DISEASE
Aetiology
• Unknown
• Various bacteria and viruses suggested
• No good evidence to suggest any of them
• Perpetuated by autoimmune response and
CD4 + T-cells
• Tumour necrosis factor (TNF) thought to be
important

84
 BEHÇET’S DISEASE
Systemic Involvement

Oral aphthous
ulceration – 100%

85
 BEHÇET’S DISEASE
Systemic Involvement
• Skin lesions – 80%
– Erythema Nodosum

– Acneiform

• Uveitis 70% (inflam. of

iris, ciliary body or
choroid)

86
 BEHÇET’S DISEASE
Systemic Involvement
• CNS involvement –
strokes, fits
• Major vessels eg
superior Vena cava
obstruction
• Increased skin
response to trauma eg
blood taking

87
 BEHÇET’S DISEASE
Ocular Features
• Acute iritis
– Pain, redness & VA
– Flare (PTN exudation)
– Inflammatory cells in
anterior chamber
– KPs (Inflammatory cells at
posterior surface of
cornea)
• Recurrent hypopyon
(Fluid level of WBC)
The red or white eye

88
 BEHÇET’S DISEASE
Ocular Features
• Marked inflammation of the
eye
• Retinal vasculitis and
haemorrhage (inflam. of
retinal vessels)
• Occlusive periphlebitis
(venous sheathing &
occlusion)
• Retinal microinfarcts
• Very damaging to vision:
retinal damage and optic
nerve atrophy
• Cataract or glaucoma

89
Vogt-Koyanagi-Harada
syndrome
Vogt-Koyanagi-Harada syndrome
 Vogt-Koyanagi-Harada syndrome
• Vogt-Koyanagi-Harada (VKH) disease is a
multisystemic disorder characterized by

• granulomatous panuveitis with exudative

retinal detachments that is often associated
with neurologic and cutaneous manifestations.
 Vogt-Koyanagi-Harada syndrome
• VKH disease occurs more commonly in patients
with a genetic predisposition to the disease,
including those from Asian, Middle Eastern,
Hispanic, and Native American populations.

• Several human leukocyte antigen (HLA)

associations have been found in patients with
VKH disease, including HLA-DR4, HLA-DR53, and
HLA-DQ4
Uveitis in Chronic
Systemic disease
Uveitis in Chronic Systemic disease
• AIDS
• Acquired syphilis
• Tuberculosis
• Leprosy
• Lyme disease
 Ophthalmic Manifestations of HIV
Infection
Anterior segment

–Molluscum Contagiosum
–Herpes Zoster Ophthalmicus
–Kaposi’s Sarcoma
–Conjunctival Squamous Cell Carcinoma
–Trichomegaly
–Dry Eye
–Anterior Uveitis
 Posterior segment
–Retinal Microvasculopathy
–CMV Retinitis
–Acute Retinal Necrosis
–Progressive Outer Retinal Necrosis
–Toxoplasmosis Retinochoroiditis
–Syphilis Retinitis
–Candida albicans endophthalmitis
•NEURO-OPHTHALMIC
Anterior Uveitis
 Anterior Uveitis
• HIV related anterioruveitis can be:

– Direct manifestation of the human immunodeficiency virus infection

– autoimmnune in origin

– drug induced ie: rifabutin, secondary to direct toxic effect upon the
non-pigmented epithelium of the ciliary body
–Any of the different infections

associated with AIDS, ie: Herpes Zoster Virus, Herpes Simplex

Virus,Cytomegalovirus, Toxoplasma gondii, Syphilis
Rifabutin induced anterior uveitis
 Retinal microvasculitis
• Retinal microvasculopathyoccurs in more than half of the patients
with HIV

transient cotton wool spots

•It is seen as (CWS),
intra-retinal haemorrhages and microaneurysm, which
occurs in 50-70% of patients. It is usually asymptomaticusually
asymptomatic.
•It has an unclear pathogenesis, but it is thought to be HIV infection of
retinal vascular cells.

•Treatment is based in delaying the progression of the disease

associated with HIV
 CMV Retinitis
• Introduction–CMV Retinitis is the commonest intraocular ocular
opportunistic infection commonest infection seen in patients with
AIDS–Antibodies are found in almost 95% of adults.

• causing a trivial illness in immuno-competen adults, however

severe immunosuppression causes viral reactivation and tissue
invasive disease

•Pathogenesis–Reactivation from extraocularsites leads to seeding in

other sites such as the retina

•Epidemiology–The number of newly diagnosed cases of CMVR has

decreased since the introduction of the HAART
 CMV Retinitis
• Clinical manifestations

• –Patients may complain of minor visual symptoms such as floaters,

flashing
• lights or mild blurred vision lights vision, or be totally
asymptomatic.
• –It presents with a wide range of clinical appearances. From cotton
wool spots which may look like HIV Retinopathy to confluent areas
of full thickness retinal necrosis and vasculitis.

• CMVR can progress in a “brushfire” pattern from the active

edge of an active lesion.
 Treatment

• –The treatment of CMVR in patients with AIDS requires the use of

specific antiviral agents, ganciclovir ganciclovir, ,
foscarnet or cidovir in conjunction with HAART.
• –These treatments can be administered orally, intravenously or
intravitreally. Systemic treatment has the advantage of treating
infection elsewhere in the body as well as the other eye but has the
disadvantages of systemic side effects.

• –Intravitrealimplants release the drug over a six-month period,

achieving prolonged high intravitreallevelsofdrug.
 Acute Retinal Necrosis
• ARN is a confluent peripheral whitening of the retina with marked
vitritisand blood vessel closure. Optic neuritis and retinal
detachment are frequent complications.

•ARN is usually due to Varicella Varicella-Zoster infection, but it can

also be caused by Herpes Simplex virus or Cytomegalovirus.

•Initially described in theimmuno-competent, it has also

been described in the immunosuppressed.

•Patients are treated with high doses of intravenousaciclovir

aciclovir or famciclovirfamciclovir, combined with laser
treatment to prevent retinal detachment.
 Progressive Outer Retinal Necrosis
(Varicella-Zoster Retinitis
• devastating viral retinitis caused by Varicella Varicella-Zoster virus
Zoster virus, without vitritisor retinal vasculitis.

•The retinitis can be located anywhere but it is common for the lesions
to coalesce and spread posteriorly in a rapid fashion.

•The main symptom is rapid loss of vision. The retina shows

typically a white lesion with no haemorrhages or exudates.

•Treatment is often unsatisfactory and usually requires combination of

Ganciclovirand Aciclovir. The prognosis is very poor and retinal
detachment is common. Resolution may leave a white plaque with the
appearance of “cracked mud”.
 Toxoplasma Retinochoroiditis
• Toxoplasmosis retinochoroiditisis an uncommon
infection of the eye in AIDS. Ocular toxoplasmosis in
HIV positive patients is different in appearance from
immunocompetentpatients.

• Unlike in immunocompetent patients, HIV infected

patients often have bilateral and multifocal disease
associated with anterior uveitis and vitritis but unlike
immunocompetentpatients, in HIV infected patients
often have with no pigmented scars adjacent to the
areas of retinal necrosis.
 Syphilis Retinitis
• There is a strong association between syphilis and HIV
infection.

•It can manifest as a retinitis with dense vitritis, retinal

vasculitis, serous retinal detachment or
neuroretinitis, as well as other types of ocular
involvement such as, conjunctivitis, anterior uveitis,
cranial nerve palsies and optic neuritis.

•Treatment consists in high dose of intravenous Penicillin

for 2 weeks.
 Neuro-Ophthalmic features
• 1. Argyll Robertson Pupil
• 2. Optic nerve Lesion
• 3. Ocular Motor Palsies
• 4. Visual Field Defects
 Ocular manifestations of
leprosy
• Chronic granulomatous inflammation caused by the acid-
fast bacillus
• Mycobacterium leprae
• (discovered by Gerhard Hernick Armauer Hansen in
Norway in 1873)
• One of the oldest recorded infections affecting humanity
(2000 BC)
• Primarily affects superficial tissues
• – Skin
• – Peripheral nerves
• Global Disease burden : 181,941 cases at the end of 2011
 Modes of ocular involvement

• Direct invasion of ocular tissue by bacilli

• Lepra reaction

• Involvement of nerves
• – Trigeminal nerve : ↓corneal sensations
• – Facial nerve : weakness of orbicularis oculi
 External structures

• Eyebrows & Eyelashes:

• Superciliary madarosis

• loss of eyebrows (lateral half)

• Ciliary madarosis

• – Loss of eye lashes

• Trichiasis
• – In turning of eye lashes
• – Rub against bulbar conjunctiva & Cornea.
• – corneal abrasions and ulcers
 Iris & Ciliary body

• Acute / Chronic inflammation can involve any part of Uvea

• Acute Iridocyclitis:
• Part of ENL reaction (Type 2 lepra reaction)
• Symptoms:
• – Pain, photophobia, redness, Lacrimation,
• – Blurring of vision
• Signs:
• – Circumcorneal congestion
• – Corneal edema, fine keratic precipitates
• – AC cells & flare
• – Miotic , sluggishly reacting pupil
• – Iris Pearls: Chalk particle like glistening lesions near pupillary
margin
 Chronic Iridocyclitis:
• Direct invasion of anterior uvea by bacilli
• Symptoms: Dull pain in the eye
• Signs:
• – Mutton fat Keratic precipitates
• – Iris atrophy & nodules
• – Pupil: miotic, non-reactive, irregular
• – Posterior synechiae
• – Complicated cataract
 Chorioretinitis
• White, waxy, highly refractile deposits at ora
serrata
• - Retinal scarring & retinal vessels sheathing
and fibrosis
• Endophthalmitis
• Panophthalmitis
 Ocular tuberculosis
• The term "ocular tuberculosis" encompasses
any infection by Mycobacterium
tuberculosis, or one of three related
mycobacteria species (sp. bovis, africanum,
and microti), in, on, or around the eye.
Historically, authors have used the terms
"primary" and "secondary" ocular tuberculosis
 Clinical Presentation

• The most common manifestation of ocular

involvement is uveitis, usually presenting as a
chronic

• anterior uveitis, panuveitis or as a choroiditis

 Lyme disease
• Lyme disease is a multi-system disorder
caused by the spirochete Borrelia
burgdorferi (B.burgdorferii) that is
transmitted to humans by the bite of a tick
with symptoms ranging from a rash, fever, and
headache to joint pain
Stage Systemic Manifestations Ocular Manifestations

I Bull's-eye rash (Erythema migrans) Conjunctivitis

Headache, malaise, and fatigue Episcleritis
(Local) myalgias, and/or arthralgias
Swelling of lymph glands near tick bite
II Migrating pains in joints/tendons Optic neuritis
Severe headache Perineuritis
Meningitis, Stiff, or Aching neck Papilledema
(disseminat Encephalitis/myelitis Optic nerve atrophy
ed) Cranial neuropathy (facial palsy) Retinal hemorrhages
Tingling or numbness in extremities Retinal vasculitis
Abnormal pulse Choroiditis
Atrioventricular block Blepharitis
Myopericarditis Exudative retinal detachments
Cystoid macular edema
Anterior or Posterior uveitis
Intermediate uveitis
Panuveitis
Endophthalmitis
Stage Systemic Manifestations Ocular Manifestations

III Oligoarthritis Chronic intraocular-

Encephalopathy inflammation

•
(Persistent)
III
Seizure, dementia,
disorientation
Keratitis
Episcleritis
• Sore throat, dry cough, or fatigue
sizziness, confusion
Spastic paraparesis, myelitis
• Nephritis or Hepatitis
Psychiatric disturbances and
Ataxia
• Testicular swelling
Lymphadenophathy
Sore throat, dry cough, or
fatigue
Nephritis or Hepatitis
Testicular swelling
Uveitis in parasitic Infection
Uveitis in parasitic Infection

• Toxoplasmosis

• Toxocariasis
Toxoplasmosis
Toxoplasmosis
• Toxoplasmosis is an infection caused by a parasite most often found
in cats and farm animals. Humans can catch this disease from:

• Coming into contact with infected cat feces

• Eating raw or undercooked meat that’s infected
• Eating contaminated vegetables or fruits
• Born with

• Note: Once a person is infected, the infection remains in the

body for life, usually in an inactive form. It can reactivate
when that person’s immune system is weak
Toxoplasmosis
 Signs and Symptoms

• Toxoplasmosis in an otherwise healthy person

may have no symptoms or only a few swollen
glands usually in the patient’s neck.

• Toxoplasmosis in a person with a weakened

immune system may only have symptoms of
swollen glands, or in the case of an infection that
attacks the brain and nervous system, the
symptoms may include fever, seizures, headache,
psychosis, and problems with vision, speech,
movement, or thinking.
Children born with Toxoplasmosis, which accounts for
about 98% of cases, may show symptoms including:
– Fever
– Swollen glands
– Jaundice
– An unusually large or small head
– Rash
– Bruises or bleeding under the skin
– Anemia
– Enlarged liver or spleen
– Seizures
– Limp muscle tone
– Mental retardation
– Hearing loss
– Vision problems (toxoplasmosis of the eye)
 Toxoplasmosis of the Eye

Congenital Toxoplasmosis is the most

common form. If the mother acquires the
infection during the first trimester, 17% of
these babies develop congenital
toxoplasmosis and the effects are severe.

However, if the infection occurs during the

third trimester, 65% of the babies develop
the disease.

The infant usually has no symptoms.

 EYE
• The parasite usually invades the retina and the choroid tissue.
Depending upon the area and severity of the infection.

• visual acuity can be unaffected to severely affected.

• The retina is inflamed by the infection and sometimes when the

inflammation settles, scars are left on the retina.

• Symptoms include floaters and blurred vision. If the scarring is on

the central macula, detailed vision will be affected.

• Approximately 35% of all retinachoroiditis cases can be attributed

to toxoplasmosis.
Active Toxoplasmosis Inactive Toxoplasmosis Scar
Effects of Ocular Toxoplasmosis
Common Effects: Occasional Effects:

– Inflammation of retina – Cataracts

– Blurred vision – The eye can be small
– Floaters – Optic atrophy
– Nystagmus – Cerebral visual
– Amblyopia impairment
– Squint
 Treatment

Treatment will not result in the elimination of the

organism from the eye. Since new lesions can form if
the organism reactivates, especially during
adolescence, patients should be closely monitored.

Medications:
– Spiramycin during pregnancy
– Antibiotics and steroid tablets during an infection
– Pyrimethamine/sulphadoxine for 6-12 months as follow-up
procedure
 Toxocariasis
• Toxocariasis is an infection transmitted from
animals to humans (zoonosis) caused by the
parasitic roundworms commonly found in
the intestine of dogs (Toxocara canis) and
cats (T. cati)
Toxocariasis
• Ocular toxocariasis: Ocular toxocariasis occurs
when Toxocara larvae migrate to the eye.

• Symptoms and signs of ocular toxocariasis

include vision loss, eye inflammation or
damage to the retina.

• Typically, only one eye is affected.

Toxocariasis
• Visceral toxocariasis: Visceral toxocariasis
occurs when Toxocara larvae migrate to
various body organs, such as the liver or
central nervous system.

• Symptoms of visceral toxocariasis include fever,

fatigue, coughing, wheezing, or abdominal
pain
 Viral Uveitis
• Herpes Zoster iritis
• Herpes simplex iritis
• Congenital rubella
 Herpes Zoster iritis

• Non granulomatous iritis

• Kps
• Iris Atrophy
• Secondary glaucoma
• Secondary cataract
• Phthisis bulbi
 Herpes simplex iritis

• Corneal lesions
• Keratitis
• Secondary Glaucoma
• Iris Atrophy
• Acute iritis
• Acute retinal necrosis
• Retinal detachment
 Congenital rubella
• Rubella is a contagious disease caused by a virus.
It is also called German measles or three-day
measles

• Congenital rubella occurs when the rubella virus

in the mother affects the developing baby at a
critical time

• In the first 3 months of pregnancy. After the

fourth month, the mother's rubella infection is
less likely to harm the developing baby.
Symptoms in the infant may include:

• Cloudy corneas or white appearance to pupil

• Deafness
• Developmental delay
• Excessive sleepiness
• Irritability
• Low birth weight
• Intellectual disability
• Seizures
• Small head size
• Skin rash at birth
 Ocular features
• Retinopathy
• Cataract
• Microphthalmos
• Glaucoma
 Fungal uveitis
• Presumed Ocular Histoplasmosis Syndrome

• Candidiasis
Presumed Ocular Histoplasmosis Syndrome
• Peripheral atrophic chorioretinal scars.

• Peripapillary scarring.

• Maculopathy.

• This condition is believed to be secondary to exposure to

Histoplasma capsulatum,

• Visual loss in POHS is secondary to the development of

macular choroidal neovascularization (CNV).
 Candidiasis
• Candidiasis is a fungal infection caused by
yeasts that belong to the genus Candida
 Treatment Uveitis
• Four types of medications

1) Mydriatics
2) Steroids
3) NSAIDs
4) Immunosuppressive medications
 Specific Strategies for Uveitis
• Type I: Eliminate agents, cromolyn, antihistamine,
corticosteroids

• Type II: Dapsone, corticosteroids, cytotoxic

agents, surgical removal
 Specific Strategies for Uveitis
• Type III: NSAIDS, corticosteroids,
immunosuppressive and cytotoxic agents,
plasmapheresis

• Type IV: corticosteroids, immunosuppressive

and cytotoxic agents, cyclosporine
 Mydriatics
• To give comfort by relieving spasm of the
ciliary muscle

• Atropine 1%, Tropicamide, Cyclopentolate

• To prevent formation of posterior synechiae

• To break synechiae
 Steroids
• Topical steroids: only for anterior uveitis

• Prednisone, prednisolone, dexamethasone

• Usually start with a high rate of instillation and

decrease as inflammation lessens

• Complications: glaucoma, posterior subcapsular

cataract, corneal complications, systemic side
effects
 Steroids
• Periocular injections

• Able to reach therapeutic concentration behind the

lens

• Longer lasting effect with depot

• Triamcinolone acetonide 40mg/ml

Methylprednisolone acetate 80 mg/ml
 Indications for periocular steroids
• Severe anterior uveitis

• Resistant cases of anterior uveitis

• Intermediate uveitis

• Poor patient compliance

• Cystoid macular edema

Systemic steroids (oral or intravenous)
 Corticosteroids
• Adverse Reactions

• Cushingoid changes (moon facies, weight gain, fat redistribution, and

increased acne)

• Delay of pubertal growth in children below 15

• Infection, hypertension, fluid retention, diabetes mellitus,

hyperlipidemia, atherosclerosis, osteoporosis, glaucoma and
cataracts

• Anxiety, sleeplessness, mood changes, easy bruising, poor wound

healing

• Pancreatitis, aseptic necrosis of bone, myopathy, psychosis

 NSAIDs

• Non-Steroidal Anti-Inflammatory agents

(NSAIDs)

• Flurbiprofen – effective in CME

 Immunosuppressive Drugs
• Indications:
• When systemic corticosteroids are insufficient
to control the disease

• Steroid side effects

• Long term use of steroids at a high dose to

suppress the inflammation
 Immunosuppressive Drugs
• Antimetabolites
• Azathioprine (Imuran)
• Methotrexate (Rheumatrex)
• Mycophenolate mofetil (Cellcept)

• T-cell inhibitors

• Cyclosporine (Sandimmune; Neoral)

• Tacrolimus (Prograf)
• Alkylating agents
• Cyclophosphamide (Cytoxan)
• Chlorambucil (Leukeran)
 Common Ophthalmic Indications for Cytotoxic
Immunosuppression
• Type I: Autoimmune diseases: few
• Type II: severe lens-induced uveitis
• Type III: Autoimmune/collagen vascular associated
disease: Bechet’s disease, PAN, Wegener’s
granulomatosis, SLE, rheumatoid arthritis
• Type IV: Autoimmune diseases: SO, VKH, birdshot
retinochoirodopathy, pars planitis
Immunosuppressive Usage & Side
Effects
Immunosuppressive Usage & Side
Effects