The document discusses various types of infectious uveitis, including bacterial, parasitic, viral, and fungal origins, with a focus on tuberculosis and its ocular manifestations. It details the clinical features, diagnostic investigations, and treatment options for conditions like syphilitic uveitis, toxoplasmosis, toxocariasis, and onchocerciasis. Emphasis is placed on treatment strategies and the importance of accurate diagnosis to avoid mismanagement.

1. INFECTIOUS UVEITIS
(PART -1)
DR. SHASHI KUMAWAT
PG FIRST YEAR RESIDENT
ESI HOSPITAL BASAIDARAPUR , NEW DELHI

2. Classification
1. Bacterial uveitis
■ Tuberculosis
■ Syphilis
■ Borreliosis ( lyme disease )
■ Brucellosis
2. Parasitic
■ Toxoplasmosis
■ Toxocariasis
■ Onchocerciasis
■ cysticercosis

3. 3. Viral
■ CMV retinitis
■ Herpes
■ Acute retinal necrosis
■ Progressive outer retinal necrosis
4. Fungal
■ Ocular histoplasmosis
■ Candida
5. Purulent uveitis and endophthalmitis

4. Tubercular uveitis
■ Tuberculosis (TB) is a chronic granulomatous infection usually caused in humans by
Mycobacterium tuberculosis.
■ It is an airborne communicable disease.
■ TB is primarily a pulmonary disease but may spread by the hematogenous route to
other sites.
■ Immune deficiency is a risk factor, when atypical mycobacteria such as M. avium
may cause disease.

5. Ocular features :
■ Anterior uveitis is very common and is usually granulomatous type. Iris nodules may be
present.
■ Choroidal granuloma ( tubercle ) : these are the focal elevated dome shaped lesions that may
be u/l or b/l and solitary or multiple . Extensive infiltration may be seen in individuals with
AIDS.a large abcess like tubercle is k/a tuberculoma. Solitary tubercular choroidal granuloma
can be misdiagnosed as choroidal melanoma due to the multiplicity of clinical findings which
also is a cause for delay in diagnosis.
■ Choroiditis independent of tubercles, typically multifocal and in a centrifugally spreading
serpiginous pattern (serpiginoid), can be seen. Choroiditis that tracks retinal vessels may have
reasonably specific for TB.
■ Vitritis is very common and may be secondary to anterior, intermediate or posterior primary
foci.
■ Macular complications include cystoid oedema and epiretinal membrane formation can be
seen.

7. ■ Retinal vasculitis is preferentially venous. Retinal haemorrhages are common.
Vascular occlusion with extensive ischaemia and preretinal or disc
neovascularization can occur. It is hypothesized that some cases of Eales disease
represent a hypersensitivity reaction to TB.
■ Other menifestations include
a. Reddish brown eyelids nodule ( lupus vulgaris )
b. Conjuctivitis
c. Phlyctenulosis
d. Interstitial keratitis
e. Scleritis
f. Exudative retinal detachment
g. Optic neuropathy include neuroretinitis

13. ■ Investigations
Confirmation of a tubercular etiology is based upon findings suggestive of systemic TB.
Mandatory investigations include:
• Routine blood hemogram
• Erythrocyte sedimentation rate (ESR)
• Mantoux tests
• Radiological imaging such as chest X-ray/CT scan.
• Newer tests based on Gamma interferon assays such as quantiFERON TB-Gold tests.

14. ■ It is to be remembered that: ELISA and PCR testing for TB on serum are not useful
especially in endemic regions such as India and do not form the basis of diagnosis
of intraocular tuberculosis.
■ FFA and ICG are useful in confirming the activity of the lesion and to identify
complications such as CNVM. A typical early hypofluorescence followed by a late
hyperfluorescence characterizes an active choroiditis and a classical ring of fire
appearance is seen in subretinal abscess and choroidal granuloma in FFA.
■ In cases of retinal vasculitis, ancillary investigations detect/confirm the presence of
neovascularization and capillary non-perfusion areas, which may need prophylactic
laser photocoagulation.
■ In cases of TB choroidal granuloma, OCT revealed an area of localized adhesion
between the choriocapillaris retinal pigment epithelial layer and the overlying
neurosensory retina (“contact” sign) and this is postulated to be due to
inflammatory adhesions overlying the granuloma that cause the neurosensory retina
to stick to the retinal pigment epithelium (RPE) at that point.

15. ■ Ultrasound (USG), B scan is a valuable tool in the diagnosis of mass like lesion such
as a large sub-retinal abscess thus ruling out neoplasia.
Treatment
■ Low-dose steroids for four to six weeks, concomitant ATT, have a protective effect
against tissue damage from delayed type of hypersensitivity reactions hence a
combination of choice.
■ Use of corticosteroids alone should be avoided as it may promote multiplication of
bacilli and even lead to panophthalmitis.

20. ■ Recent Advances
• Fourth generation quinolones, rifabutin and macrolides are part of ATT regimes
especially in multidrug resistant (MDR) – TB.
• Usefulness of retinal amine in patients with TB chorioretinitis is being evaluated.
• Surgery is reserved for complications.

21. Syphilitic uveitis
■ It is caused by the spirochete treponema pallidum.
■ It is spread by : sexual contact
: blood transfusions
: placental spread to the fetus
■ 3 clinical stages
• Primary syphilis is characterized by a painless ulcer (chancre), commonly on the genitalia . Spontaneous
resolves after 4 to 6 weeks.
• Secondary syphilis consists of a maculopapular rash and other systemic features like fever malaise is present.
Most infectious stage with the highest systemic load. Ocular involvement occur in approx 10% of the pt.
• Latent syphilis.
• Tertiary syphilis occurs in about 40% of untreated cases and is characterized by soft tumor like areas of
inflammations k/a gummas . cardiovascular manifestations such as aortitis, neurosyphilis and gummatous
infiltration of bone and viscera can be seen.

24. investigations

26. Toxoplasmosis
■ Toxoplasmosis is a common zoonosis caused by Toxoplasma gondii, and it is one of
the most important causes of infectious retinal disease and posterior uveitis.

27. ■ The retina is the primary site of T. gondii infection in the eye and the hallmark is a
necrotizing retinochoroiditis satellite to old hyperpigmented scars and accompanied
by vitreous and anterior inflammation. Retinal vasculitis is also present.

28. ■ The most common clinical signs of active ocular toxoplasmosis are blurring or loss
of vision and floaters. Depending on the location of the lesions and the anterior
chamber and vitreous inflammation, patients can be more or less symptomatic.
■ ‘Spill-over’ anterior uveitis is common. It may be granulomatous .
■ A single inflammatory focus of fluffy white retinitis or retinochoroiditis associated
with a pigmented punched out scar (‘satellite lesion’) is typical. Lesions tend to
involve the posterior pole.
■ Vitritis may be severe and impair fundus visualization. ‘Headlight in the fog’ is the
classic description of a white retinal inflammatory nidus viewed through vitritis.
■ Optic disc oedema is common.

33. ■ In most cases toxoplasmic retinochoroiditis is a self-limited disease. Untreated
lesions generally begin to heal after 1 or 2 months, although the time course is
variable, and in some cases active disease may persist for months.
■ As a lesion heals, its borders become more defined, and after several months may
become hyperpigmented. Large scars will have an atrophic center that is devoid of
all retinal and choroidal elements; the underlying sclera gives the lesion its white
center.
■ Recent evidence has also suggested that patients with recent acquired infection
may present with vitritis or even anterior uveitis in the absence of retinochoroiditis.

35. The combination of pyrimethamine, sulfadiazine, and corticosteroids, which is considered “classic” therapy
for ocular toxoplasmosis , is the most common drug combination used and considered the best option.

37. ■ Local treatment with intravitreal injections of clindamycin and dexamethasone
without concomitant systemic therapy is a treatment option in pregnancy or patients
with allergies or inadequate responses to oral medications.
■ Pregnant women with toxoplasmic seroconversion should be treated with systemic
spiramycin to reduce the risk of congenital disease.
■ However, if congenital toxoplasmosis is identified by fetal ultrasound or amniotic
fluid PCR, classic therapy that crosses the placenta should be prescribed.

39. Ocular toxocariasis
■ Toxocariasis is an infection caused by the nematode T. canis and by other
roundworms such as T. cati.
■ Systemic effects of Toxocara infestation in the human are termed visceral larval
migrans (VLM).
■ VLM is usually a self-limited disease and typically affects young children from 6
months to 4 years of age. In contrast to visceral toxocariasis, ocular larva migrans
tends to occur in older children and adults.
■ Humans can be infested by ingestion of embryonated eggs or larvae. Eggs can be
ingested accidentally after contact with puppies or by geophagia of soil containing
embryonated eggs.

40. Clinical presentation
■ The ocular involvement is typically unilateral,
■ Patients usually present with unilateral visual impairment, leukocoria, and/or
strabismus in a relatively quiet eye.
■ Based on ophthalmoscopic findings, ocular toxocariasis can be classified into these
categories: 1. peripheral granuloma
2. posterior pole granuloma
3. chronic endophthalmitis
4. atypical presentations

41. ■ Peripheral granuloma presents as a dense, white inflammatory mass in the
periphery of the retina. The prognosis in eyes with peripheral granulomatous
inflammation is usually relatively good and visual acuity can be preserved.

42. ■ Posterior pole granuloma presents as white or gray spherical intraretinal or
subretinal granuloma affecting the posterior pole. Most of the time it is diagnosed in
a cicatricial stage when the lesion appears as a well-defined subretinal mass,
measuring from 500 to 3000 µm, with no hemorrhage or exudates.

44. ■ Chronic endophthalmitis typically presents with leukocoria, strabismus, floaters or
unilateral visual loss.
■ Features may include anterior uveitis, vitritis, chorioretinitis, papillitis and a fundus
granuloma .
■ A dense greyish-white exudate, similar to the snowbanking seen in PP, may involve
the peripheral retina and pars plana.
■ Complications leading to a poor visual outcome include tractional retinal or ciliary
body detachment with hypotony leading to phthisis bulbi.

45. Investigation
■ It is particularly important to distinguish a Toxocara granuloma from
retinoblastoma. Other helminthic organisms can give similar clinical manifestations.
• Full blood count. Eosinophilia may be present, particularly in visceral larva migrans
and can become chronic.
• Hypergammaglobulinaemia especially IgE.
• Serology. Antibodies to Toxocara canis are detectable in only about 50% of ocular
cases.
• Ultrasonography may be useful if the vitreous is hazy.
• Aqueous or vitreous sampling for eosinophilia, antibody detection and PCR.
• Biopsy of a granuloma of the skin or elsewhere for larvae is sometimes possible

46. Ocular treatment
• Prevention by good hygiene practices and deworming of pets.
• Steroids. Topical, regional and systemic may be considered.
• Anthelmintic agents such as mebendazole and thiabendazole can be considered in
ocular toxocariasis, remembering that worm death may promote inflammation.
• Vitrectomy for sight-threatening tractional sequelae.

47. Onchocerciasis
■ Onchocerciasis, which affects the eyes and skin, is the second most common cause
of infectious blindness in the world.
■ The parasitic helminth Onchocerca volvulus is causative.
■ The vector is the Simulium blackfly, which breeds in fast-flowing water, hence the
colloquial term ‘river blindness’.
■ Larvae are transmitted when the fly bites to obtain blood.

48. Clinical features
■ Systemic features are principally dermatological and include pruritus, a
maculopapular rash (onchodermatitis) involving the buttocks and extremities and
areas of hypo- and hyperpigmentation on the shins (‘leopard skin’ –). Scratching of
itchy areas leads to lichenification.
■ Onchocercomata are non-tender subcutaneous nodules that enclose 2–3 adult worms.
■ Live microfilariae may be seen in the cornea, vitreous and suspended in the AC after
the patient has postured facedown for a few minutes followed by immediate slit lamp
examination.
■ Anterior uveitis is an early feature. Pear-shaped pupillary dilatation may be seen and
is due to PS.
■ Keratitis. Punctate keratitis (snowflake opacities) affects a third of patients and
consists of infiltrates surrounding dead microfilariae.
■ Chorioretinitis is usually bilateral and predominantly involves the temporal fundus,
sparing the macula until late.

50. Treatment
■ Ivermectin kills microfilariae (but not adult worms) and is given at least annually for
many years. Ivermectin occasionally precipitates inflammation, so prophylactic
prednisolone may be considered in patients with visible AC microfilariae.
■ Moxidectin is a newer drug that may be superior to ivermectin.
■ Doxycycline 100–200 mg per day for 6 weeks targets Wolbachia, indirectly
preventing microfilarial embryogenesis.
■ Suramin is effective against adult worms. It is given intravenously.
■ Steroids. Anterior uveitis is responsive