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Caused by bacillus Mycobacterium tuberculosis PRIMARY : there are no other systemic lesions SECONDARY : infection resulting from contagious spread from adjacent structure or by hematogenous spread
EPIDEMOLOGY • First described in eye by Maitre-Jan in 1711 who identified an iris lesion and attributed it to the disease • Incidence: ranges from 1.4 - 5.74% • No racial preferences • No sexual predilection • Elevated rates of TB infection are seen in individuals immigrating from Mexico, Philippines, Africa, Southeast Asia, the Caribbean, and Latin America.
lymphocytes. Their antigenicity is due to multiple cell wall constituents. which activate Langerhans cells. including glycoproteins. usually via hematogenous routes. • Mycobacteria are highly antigenic. M tuberculosis is able to invade local lymph nodes and spread to extrapulmonary sites. and they promote a vigorous.Because of the unique ability to survive and proliferate within mononuclear phagocytes. and wax D. and polymorphonuclear leukocytes. phospholipids.Pathophysiology: • M tuberculosis is a slow-growing obligate aerobe. nonspecific immune response. .
lacrimal sac and conjunctiva • lid abscesses • tarsitis 2) Conjunctiva: chronic conjunctivitis Primary: Unilateral. with swelling and caseous preauricular and sub maxillary LN • Conjunctiva becomes hypertrophied and large follicles appear which may break down and ulcerate. < 20 yrs. mucoid secretion and conjunctival and lid oedema. • lacrimation. .C/F External ocular findings: 1) Eye lids: • Lupus vulgaris -lids.
• May present in any 1 of the 6 forms: 1. • No associated LN enlargement. Small millet seeded ulcers which may or may not coalesce 2. Small grayish sub conjunctival tubercles 3.Secondary: • Bilateral. lacrimal gland. previously infected pts. • Results due to the infection of the conjunctiva from a contagious TB focus-TB lid. orbit. with proliferative changes and large cockscomb excrescences. age > 20 yrs. A hypertrophic form. tarsus. .
. Lupus conjunctiva associated with lupus of the skin. Pedunculated polyps arising from the tarsal or fornicial conjunctiva. 5. 6. Tuberculoma of the conjunctiva.4.
• A leash of blood vessels may extend from the conjunctiva to the cornea giving the so-called fascicular keratitis. adjacent to the limbus. TB • Typically. • Photophobia. The child keeps his lids closed and tries to seek dark corners. . conjunctival injection and lacrimation are common symptoms.seen in children • On the bulbar conjunctiva.Phlyctenulosis • Allergic response to the Myco.
• They are often not solitary. • Recurrences are very common. full recovery occurs. the phlyctenules sink to the level of the conjunctiva and quickly epithelise over. • Corneal perforation is a very rare .• Within 2-3 days the small greyish masses break down. small pits appear at the apex. • Decreased vision may be due to dense corneal scarring with pannus. • If cornea is not involved there is no scarring.
This localized inflammation may later become intense. • Arise either as an extension of TB scleritis or from the bacilli from the Schlemm’s canal producing corneal lesions • Initially there is deep. • The attack may heal by corneal scarring or may progress to severe keratitis or kerato-uveitis and produce blindness .Cornea: Sclero keratitis : • Marginal keratitis with involvement of the contagious sclera. vascular congestion at the limbus followed by the appearance of corneal infiltrates.
. • Healing is by scarring or calcareous degeneration of the cornea causing loss of vision. involving the lower 2/3rd. • Gradual onset with slow involvement of the cornea. • Characteristic superficial vascularisation with occasional deep vascularisation • Prolonged course with frequent exacerbation and remissions.Interstitial keratitis • extend from sclero-keratitis or progression of disease from uveal focus. • Diffuse corneal infiltrates with intracorneal nodules – real tubercles. • Peri-corneal inflammation-mild to moderate.
• Healing is by scarring or calcareous degeneration of the cornea . which gradually spreads to the upper and middle layers leaving a marginal peripheral area clear. • Corneal sensations +++ • Characteristic deep vascularisation which may proceed to superficial layers in the late stages. Descemet’s membrane and parenchyma of the cornea. • Infiltration confined to the deep layers of the central cornea.Deep central keratitis • Arise from the bacilli in the aqueous which penetrate the corneal endothelium.
ulceration and sloughing or healing by severe scarring with loss of vision . • These infiltrates may either undergo necrosis. whitish infiltrates with illdefined borders and often an opaque halo which merges into clear cornea. • Appear as small.infiltrates of the cornea • Seen in older age groups. localised.
• Secondary infection of the ulcer is common. • Ulcer may progress and perforate the cornea leading to loss of vision . • TB bacilli are found in the scrapings. relentless and destructive ulcer extending from the limbus with sloping edges and have a caseous base.corneal ulcers • Exremely rare condition. • Progressive.
Involves characteristically 1 sector of the sclera. • Scleral perforation does not occur. succulent oedematous inflammation of both the sclera and episclera. a diffuse. . there is brawny scleritis. • In the malignant form.Sclera • May cause episcleritis or scleritis Anterior Scleritis • Most frequent type • Appears as a deep. purplish-red congestion which does not fade on the injection of ephedrine into the conjunctival sac.
Posterior scleritis • Affects the sclera posterior to the equator + Tenon’s capsule = sclero-tenonitis. • Proptosis and ocular immobility disappear as the secondary tenonitis fades . mild-moderate proptosis and decreased eye movts. little or no anterior inflammation. • Characterised by lid oedema. • Moderate pain during the acute stage of tenonitis.
thickened iris. Synechiae. loss of normal iris pattern and iris lustre. prescence of the Koeppe’s nodules at the pupillary margin. . • Capsular clouding of the lens and • secondary glaucoma occurs. • Both the Anterior and the posterior uvea may be involved independently Anterior TB Uveitis: Tuberculous granulomatous uveitis: Slow onset • Peri-corneal congestion. severe post. • Mode of spread = haematogenous spread.uveal tract • A TB focus may probably be the starting point from which all the other types of endogenous ocular TB arise. muttonfat KPs.
Anterior uveitis .
Nodular Tuberculous Iritis • • • • miliary tubercles on the iris. Occur in pts with low sensitivity to tuberculin Insidious onset with minimal inflammation Tubercles appear as small greyish nodules. either in the superficial iris or in the iris stroma with little surrounding inflammatory reaction Conglomerate tubercle of the iris • Rare condition • Results either from a forward extension of ciliary tubercle or from the fusion of miliary tubercles • Appears as a large. • Pain is constant • Very poor prognosis . invasive malignant tumour located at the angle of the AC.
Posterior TB uveitis Circumscribed choroiditis • • • • Usually affects the individual > 20 yrs age Has a predilection to involve macula. the lesion becomes more well defined. • Recurrences are frequent. Initially ill defined lesion in the posterior pole In 6 wks. appear at the periphery of the old lesion . becomes circumscribed and healing appear with pigment around the lesion and secondary gliosis. • Within 3-4 mths the lesions appear healed.
Spreading choroiditis Devastating form of choroiditis seen in<20 yrs having high sensitivity and low immunity. • rapid inflammation and exudations, starting as a small focus spreading over the entire fundus and overlying retina. • There is clouding of the vitreous and decreased vision. • Necrosis and caseation always occur • Finally, there is wide spread atrophic choroiditis, with pigment heaping, gliosis of the choroid and retina and exposure of the choroidal vessels.
Miliary TB of the Choroid
• Terminal complication of the TB meningitis. • multiple, 1-3 or more in number, appear as small yellowish- pink nodules with little or no evidence of surrounding inflammation. • Characteristically seen in the posterior pole of the eye
Solitary tubercles of the Choroid
• in adults having low sensitivity and high immunity.pearlywhite or greyish masses • Little or no vitreous clouding is seen. • Tubercles usually heal by hyalinization, the inflammatory reaction may become intense and a conglomerate tubercle of the posterior segment may form.
• Conglomerate tubercle of the posterior segment
Extremely rare, break down of a solitary tubercle, appears as a large mass covered with exudate and H’hages, retina becomes detached and vitreous clouding is present. • Necrosis and caseation are rapid.
• Pars plana "snowbanking" or granulomas can be seen. . especially if it is unilateral.Vitreous findings • Anterior vitreous cell with the development of cellular aggregates known as "snowballs" in the anterior and inferior vitreous. • TB is an important diagnosis in the differential of pars planitis syndrome.
Superficial multiple or single exudates in the retina 2. multiple rather circumscribed exudates .TB retina secondary to choroidal TB 2 forms : 1. TB periphlebitis Exudative retinitis • haematogenous spread in adults having low moderate tuberculin hypersensitivity • superficial.
Periphlebitis: • • • • • Most frequent cause of Eales’ disease Common in India & middle east M>F 20-30 yrs 80-90% BL extensive vascular sheathing .
focal sepsis .Clinical course: • Stage of inflammation • Stage of ischemia/ non perfusion • Stage of neovascularization with/ without sequalae Etiology: • Unknown • Assoc with TB. thrombangitis oblterans .
C/f Stage of inflammation: • • • • • • • • Vascular sheathing Exudates Retinal h’age Vitreous cells Macular oedema Epiretinal membrane AC flare KP .
Stage of nonperfusion • • • • Obliterated vessels A-V shunts BRVO Demarcation bet perfused and non perfused areas .
Stage of neovascularization: • • • • • NVD NVE Haemorrhages Fibrovascular proliferation Tractional retinal detachment .
systemic Used in inflammatory phase . sub tenon’s.Management AIMS: • Reducing vasculitis and vitritis • Reducing risk of vit h’age • Removing nonresolving vit h’age Mainstay of t/t is STEROIDS Topicals .
1% Peribulbar Triamcinolone Oral Prednisolone 1-1.Steroids: Topicals: predacetate 1% Dexamethasone 0.5 mg/kg/day .
vascular leakage.capillary closure. venous beading and early NVE .
• Tubercles are found along the pial coat and may even be present along the intra septal pial extensions into the nerve substance. • Necrosis and caseation follow with complete destruction of the nerve occurs ultimately leading to complete optic atrophy • TB optic neuritis may occur following retinal periphlebitis as well .Optic nerve TB optic neuritis • complication of TB meningitis in 10-60% of the cases.
Papillar edema .
• Optic atrophy occurs with progressive necrosis and caseation of the optic nerve. .Neuro-ophthalmic disease: Tuberculous meningitis • Raised ICT will lead to VI and III CN palsies.
Requires density of 5. aqueous or vitreous specimens are used • 2) Culturing: • more sensitive and can detect densities of 10-100 bacilli per ml .INVESTIGATIONS: • • DEFINITIVE DIAGNOSIS PRESUMPTIVE DIAGNOSIS DEFINITIVE DIAGNOSIS: 1) Microscopy: • • easiest but least sensitive test.000 to 10.000 bacilli per ml.
Colonies of myco tuberculosis on L-J medium Acid fast stain .
3) PCR:to amplify mycobacterial DNA Presumptive diagnosis • relies on a combination of features including the clinical picture. evidence of disease elsewhere and evidence of previous tuberculous infection. sent for microscopy. culture and PCR . 1)Radiology: can show both active and old pulmonary tuberculosis 2) Extra-ocular tissue specimens : serial sputum samples. broncho-alveolar lavage. transbronchial biopsy.
3) Tuberculin skin testing: • Mantoux test: reaction depends on delayed-type hypersensitivity and therefore is testing whether the patient has an acquired specific immune response to the bacillus .
5) Other tests: Interferon gamma titers .4) OCT : choroidal lesions highlights an elevated choroid with localized contact of the choriocapillaris-retinal pigment epithelial complex with subretinal fluid.
6) Indocyanin green angiography: both for diagnosis and monitoring the effect of t/t Hypofluorescent spots .
Assessing the ocular complications of anti.Ophthalmologists are involved in three aspects of tuberculosis (TB) management: • 1. .tuberculous medication. Screening known tuberculosis patients for ocular manifestations of the disease. • 3. Diagnosing ocular tuberculosis in patients presenting with eye problems. • 2.
Treatment: Medical t/t 1) Patients ocular inflammation and who have a recent skin test conversion. except ethambutol may be left off and t/t is required for 9 months. Isoniazid and rifampin are continued for an additional 4-7 months for a total duration of therapy of 6-9 months. For ocular TB with extrapulmonary involvement and without pulmonary involvement. and pyrazinamide for 2 months. chest x-ray. A 4-drug regimen is given:Isoniazid. rifampin. or systemic findings consistent with TB clearly need t/t of pulmonary TB. t/t same. positive sputum cultures. . ethambutol. Ocular inflammation improves with systemic treatment. then ethambutol and pyrazinamide are discontinued.
. or difficult to manage with local and systemic immunosuppressive drugs or if the uveitis is sight threatening. while rifampin and pyrazinamide may be used for sterilization. progressive. then anti-TB therapy should be considered. Isoniazid initially decreases bacterial load by bacteriocidal activity. o If the uveitis is severe. o There is need of a bacteriocidal agent and a sterilizing agent.2) Patients with uveitis: ocular inflammation positive TB skin test with no systemic associations. and negative chest x-ray anti -TB antibiotic t/t is considered.
the addition of pyrazinamide is done . For iris nodules/ciliary body masses. a 2-drug regimen of isoniazid (300 mg/d) and rifampin (600 mg/d) for 9-12 months is advocated .3) With no other evidence of TB other than ocular with positive PPD.
headache.Ocular toxicity of anti-TB drugs Ethambutol: • causes dose dependent optic neuritis (focal areas of papillomacular axonal swelling and occasional demyelination. scotomas) • pts with renal insufficiency at risk • gout or hyperuricemia. GI disturbances. and disorientation. confusion. and peripheral neuritis .
• administer pyridoxine (vitamin B-6) in individuals with poor nutrition or predisposed to developing neuropathy .Rifampin: Liver damage in pre-existig liver disease INH: • may cause optic neuritis but is rare.chr alcoholics and malnourished people at risk.
. lid glands. eyelids. lacrimal drainage system. leprae antigens and due to formation of intravascular immune complexes • Secondary lesions following granulomatous infiltration of the V and VII cranial nerves • Secondary lesions following granulomatous infiltration of contiguous structures – eyebrows.OCULAR LEPROSY The ocular lesions of leprosy can be classified into 4 categories: • direct invasion of the eye by M. leprae • sensitization of ocular tissue to M.
• Caused by M. Leprae • Seen mostly in tropics and subtropical areas • 25% cases show ocular involvement 2 main types: • Tuberculoid leprosy (TT) • Lepromatous leprosy (LL) .
secondary glaucoma • Grade-V : burnt out disease. Scleritis • Grade IV : perforation of cornea. development of unilateral or bilateral phthisis bulbi . iridocyclitis.s/s • common with the lepromatous type of leprosy Grading of Eye signs: • Grade-I:Insensitivity of cornea is sight threatening lesions (STL) but not very severe in itself • Grade-II :Lagophthalmos .not serious but causes exposure keratitis • Grade III : Keratitis. Iritis.
Lids & conjunctiva • • • • • Chronic conjunctivitis severe lagophthalmos Loss of lashes (Madarosis) Trichiasis Tylosis Tylosis .
Bilateral total loss of brows and madarosis .
Corneal signs: • exposure keratitis due to the paralysis of one or both orbicularis muscles as the facial nerve is affected. • Superficial punctate keratitis in LL • Grey spots of infiltration • The ‘minute grains of chalk’ appearance in the cornea : pathognomonic of leprosy • chronic interstitial keratitis may develop • Corneal sensations are lost Leprous pannus • corneal nerves thickening or beading earliest detectable ocular findings .
Superficial punctuate keratitis Beading of corneal nerves .
pearls slowly enlarge and coalesce become pedunculated and drop into AC • Iris atrophy and miotic pupil • caused by the immune complex deposition in the uvea associated with systemic symptoms such as fever and swelling of skin lesions • large granuloma.Episclera and sclera • Episcleritis • Small episcleral nodules at the limbus Iris 1) Iridocyclitis : of chronic nature • pathognomonic sign: glistening ‘iris pearls’ at the pupillary margin. leproma may occur in AC • Poor prognosis .
scleritis iridocyclitis .
Iris atrophy and miotic pupil Specific grey spots in iris .
Other features • Small nodules may be seen in the periphery in the anterior choroid occasionally • Lacrimal glands are occasionally enlarged leading to lepromatous dacryoadenitis • Secondary cataract and glaucoma .
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