Infectious uveitis (part-1).pptx ppt upload

Uvea

1. Infectious uveitis (part -1) DR. SHASHI KUMAWAT PG FIRST YEAR RESIDENT ESI HOSPITAL BASAIDARAPUR , NEW DELHI

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

3. Viral CMV retinitis Herpes Acute retinal necrosis Progressive outer retinal necrosis 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.

6. 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 Reddish brown eyelids nodule ( lupus vulgaris ) Conjuctivitis Phlyctenulosis Interstitial keratitis Scleritis Exudative retinal detachment Optic neuropathy include neuroretinitis

7. 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.

8. 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.

9. 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 .

10. 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.

11. 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.

12. investigations

13. 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.

14. 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.

15. 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 .

16. 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.

17. 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.

18. 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.

19. 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.

20. 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

21. 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.

22. 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.

23. 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.

24. 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

25. 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.

26. 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.

27. 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.

28. 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