Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Idiopathic intracranial hypertension wikipedia , lookup
Retinal waves wikipedia , lookup
Vision therapy wikipedia , lookup
Blast-related ocular trauma wikipedia , lookup
Macular degeneration wikipedia , lookup
Diabetic retinopathy wikipedia , lookup
UVEITIS Inflammation of the uveal tract ANATOMICAL CLASSIFICATION Anterior uveitis : inflammation of iris. Intermediate uveitis : inflammation of the ciliary body and vitreous. pars planitis ( idiopathic ). Posterior uveitis : inflammation of the choroid. Panuveitis : inflammation of the whole uveal tract. ETIOLOGIC CLASSIFICATION Infectious uveitis: viral, bacterial, parasitic. Noninfectious uveitis: Autoimmune HISTOLOGIC CLASSIFICATION Nongranulomatous uveitis ( NGU ) is more common, often acute and involves anterior segment of the eye with lymphocyte and plasmocyte infiltration and a tendency to develop hypopyon and keratic precipitates K.Ps. NGU is often noninfectious and develops as a hypersensitivity reaction. GRANULOMATOUS UVEITIS Often chronic, painless and insidious, can involve any part of the uveal tract but has a tendency for posterior segment involvement. Pathologically it has infiltration of epithelioid and giant cells surrounded by lymphocytes. Large mutton fat keratic precipitates K.Ps are seen on slit lamp examination. GRANULOMATOUS UVEITIS Common infectious etiologies are toxoplasmosis and tuberculosis. Noninfectious causes are sarcoidosis, vogt koyanagi harada and sympathetic ophthalmia. UVEITIS Although the term UVEITIS refers primarily to inflammation of the uveal tissue,adjacent sructures such as the retina,vitreous,sclera and cornea are also frequently involved secondarily in the innflammatory process. UVEITIS UVEITIS is responsible for 10% of blindness. Among patients with UVEITIS about 75% have anterior uveitis ( iritis, iridocyclitis ) 8% intermediate uveitis (pars-planitis ) 17% posterior or panuveitis. UVEITIS SIGNS Autoimmune uveitis tends to be bilateral. Unilateral uveitis is often infectious. However both etiologies can be unilateral or bilateral. CLINICAL FINDINGS IN ANTERIOR UVEITIS Pain Photophobia Lacrimation Congestion Reduced vision Systemic symptoms may be present if there is association with systemic disease. CLINICAL FINDINGS IN POSTERIR UVEITIS Reduced vision. Floaters. Pain and congestion usualy are not seen. Systemic findings may be present if there is association with systemic disease. SIGNS in ANTERIOR UVEITIS Reduced corrected vision Pupillary constriction Perilimbal congestion Cornea: keratic precipitates, edema Anterior chamber: aqueous flare, cell Iris: nodules, posterior synechia Crystalline lens: pigment deposits, cataract ANTERIOR UVEITIS SIGNS CELLS seen in anterior chamber are seen in anterior uveitis and iridocyclitis. FLARE seen in anterior uveitis and iridocyclitis is the result of increased permeability of iris vessels and protein leak in anterior chamber. SIGNS IN UVEITIS Iris nodules usually seen in granulomatous uveitis can be present in different locations of the eye. BERLIN nodules are inflammatory nodules of the iris and are located in anterior chamber angle. BUSSACA nodules are seen in iris stroma. KOEPPE nodules are inflammatory nodules located in pupillary margin. ANTERIR UVEITIS: (AUTOIMMUNE ) IS THE MOST COMMON FORM OF UVEITIS. BECAUSE UVEITIS MAY OCCUR SECONDARILY TO INFLAMMATION OF THE CORNEA AND SCLERA, THE PHYSICIAN SHOULD EVALUATE THESE STRUCTURES CAREFULLY TO RULE OUT A PRIMARY KERATITIS OR SCLERITIS. ANTERIOR UVEITIS HLA-B27 ASSOCIATED UVEITIS. JUVENILE IDIOPATHIC ARTHRITIS( chronic). FUCH’S HETEROCHROMIC IRIDOCYCLITIS. PHACOGENIC UVEITIS( lens-induced ). TUBULOINTERSTITIAL NEPHRITIS and UVEITIS SYNDROME. HLA-B27 ASSOCIATED UVEITIS ANKYLOSING SPONDYLITIS REITER SYNDROME( REACTIVE ARTHRITIS SYNDROME ) IS SECONDARY TO INFECTION BY : UREAPLASMA UREALYTICUN, CHLAMYDIA, SHIGELLA, SALMONELLA, YERSINIA ORGANISMS, INFLAMMATORY BOWEL DISEASE PSORIATIC ARTHRITIS INTERMEDIATE UVEITIS Idiopathic :( Pars planitis ) is the most commom form that constituting 85%-90% of cases. Secondary : Lyme disease Syphilis Tuberculosis Multiple sclerosis Sarcoidosis Toxocariasis POSTERIOR UVEITIS Toxoplasmosis Toxocariasis Tuberculosis Sarcoidosis Vogt-Koyanagi-Harada Syndrome Sympathetic Ophthalmia AIDS related Bird shot Retinochoroiditis Behcet Syndrome, Lymphoma AIDS RELATED UVEITIS Cytomegalovirus HSV HZV Treponema pallidum Tuberculosis Cryptococcus neoformans POSTERIOR UVEITIS SIGNS Funduscopic examination : Optic nerve congestion. Macular edema. Vascular sheathing ( vasculitis) Retinal infiltration,pigmentary changes,exudation,snow balls and snow banking, intravitreal bands ,retinal detachment,retinal and macular scars and optic atrophy in chronic cases. LOW VISION IN ANTERIOR UVEITIS CORNEA : Epithelial lesions and defects, particularly in some cases like herpes virus and herpes zoster infection Edema: increased intraocular pressure,ocular hypotension. Keratic precipitates: deposits of inflammatory cells on corneal endothelium Corneal opacities and scars: in chronic cases Band keratopathy: seen in chronic cases such as cases associated with pauciarticular juvenile idiopathic arthritis UVEITIS: ( LOW VISION ) Retinal infiltrations can be infectious as in: Toxoplasmosis, tuberculosis, Toxocariasis, and varicella-zoster virus infection ( Acute retinal necrosis ). They can also be noninfectious and immune related as in: Behcet disease, sarcoidosis and white dot syndromes. UVEITIS: ( LOW VISION ) Retinal vasculitis is seen in sarcoidosis, wegner granulomatosis,lupus,polyarteritis nodosa,multiple sclerosis and numerous fungal,parasitic,bacterial,viral and rickettsial diseases UVEITIS: (LOW VISION ) Reduced vision is noticeable in posterior uveitis only if macula is involved in the process of infiltration,ischemia, exudation and edema in active uveitic syndromes. Macular traction, pigmentary changes,macular scar and macular hole are permanent changes that are seen in chronic cases of posterior uveitis. UVEITIS: ( LOW VISION ) Optic nerve involvement may also contribute to reduced vision in uveitic syndromes. Optic neuropathy can present as papillitis, papilledema,optic nerve infiltration and ischemia. Optic atrophy may be seen as a sequela of any of the above conditions in posterior uveitis. UVEITIS: ( LOW VISION ) Attacks of anterior uveitis and iridocyclitis if associated with prolonged periods of poorly controlled high intraocular pressure may leave the optic nerve atrophic and pale and lead to permanent vision loss. Optic nerve atrophy is often detectable in funduscopic examination and perimetry is only required to confirm doubtful cases. UVEITIS: ( LOW VISION ) Clinical examination including slit lamp biomicroscopy and funduscopy recognize the cause of low vision in uveitis. In some cases special diagnostic tests such as fluorescein angiography, perimetry, ultrasonography and optical coherence tomography are needed to determine the cause of low vision as well as the degree of contribution of each structure in reducing vision. UVEITIS IN ABOUT HALF OF CASES OF UVEITIS NO SPECIFIC ASSOCIATION IS FOUND AND UVEITIS IS PRESUMED TO BE IDIOPATHIC BACTERIAL UVEITIS SYPHILIS: treponema pallidum LYME DISEASE: borrelia burgdorferi LEPTOSPIROSIS:gram-negative spirochete Leptospira interrogans OCULAR NOCARDIOSIS: Nocardia asteroides TUBERCULOSIS: Mycobacterium tuberculosis OCULAR BARTONELLOSIS: Bartonella henselae is the principal etiologic agent of cat-scratch disease WHIPPLE DISEASE: Tropheryma whipplei SYPHILITIC UVEITIS SYPHILIS : is caused by spirochete TREPONEMA PALLIDUM Congenital : transplacental infection of the fetus after tenth week of gestation. Acquired : sexual contact. Diagnosis is important because syphilis can mimic any kind of intraocular inflammation that is curable and has definitive antibacterial treatment. Uveitis can occur at any stage of the disease including tertiary syphilis SYPHILITIC UVEITIS Ocular manifestations of syphilis are protean and affect all structures including the conjunctiva, sclera, cornea, lens, uveal tract, retina, retinal vasculature, optic nerve, cranial nerves, and pupillomotor pathways. Intraocular inflammation may granulomatous or nongranulomatous, unilateral or bilateral, and it may affect the anterior, intermediate, posterior segment. SYPHILITIC UVEITIS Primary syphilis may be diagnosed by direct visualization of the spirochete with dark- field microscopy. Serodiagnosis is performed by VDRL, RPR and FTA ABS test. Testing for HIV should be performed in all patients with syphilis. TUBERCULOUS UVEITIS Ocular manifestations of TB may result from active infection or an immunologic reaction to the organism. Tuberculous uveitis is classically a chronic granulomatous disease that may affect the anterior and/ or posterior segments withmutton fat K.Ps, although a nongranulomatous uveitis may occur. Disseminated choroiditis is the most common presentation of TB and is characterized as multiple, deep, yellowish lesions as tubercles. TB UVEITIS Definitive diagnosis of TB requires the findjng of mycobacteria in body fluids and tissues. This approach is not often possible, and the diagnosis is instead presumptive, based on indirect evidence. A positive result on the PPD test or intrferon gamma release assays such as the QuantiFERONTB Gold test is indicative of prior exposure to TB. AUTOIMMUNE PANUVEITIS Sarcoidosis Sympathetic Ophthalmia Vogt-Koyanagi-Harada Syndrome Behcet Disease SARCOIDOSIS A multisystem granulomatous disorder of unknown etiology with protean systemic and ocular manifestations. Although intrathoracic manifestations are most common (90%), other organs frequently involved include the lymph nodes, skin, eyes, CNS, bones and joints, liver and heart. Ocular involvement may be seen in up to 50% of patients with systemic disease, with uveitis being the most frequent manifestation. SARCOIDOSIS In most large series sarcoidosis acccouts for up to 10% of all cases of uveitis. Both sexes are affected, albeit with a slight female predominance, onset usually occurs between the ages of 20 and 50 years. Pediatric involvement is uncommon and the clinical course is atypical. Sarcoidosis can present as any kind of uveitis. SARCOIDOSIS Anterior uveitis presenting as granulomatous iridocyclitis is the most common ocular lesion. Although cornea is infrequently involved, corneal infiltrates may be seen, band keratopathy may develop either due to chronic uveitis or hypercalcemia. Posterior segment lesions occur in up to 20% of patients with ocular sarcoidosis. SARCOIDOSIS Vitreous involvement manifests as inflammation with snowballs appearing as intermediate uveitis. Perivascular sheathing apperas as periphlebitis. Irregular nodular granulomas along venules have been termed candle-wax drippings, or taches de bougie. Occlusive retinal vascular disease, especially branch retinal vein occlusion, and less commonly central retinal vein occlusion and peripheral retinal capillary nonperfusion may lead to retinal neovascularization and vitreous hemorrhage. FORMS of SARCOIDOSIS LOFGREN SYNDROME:uveitis plus erythema nodosum, febrile arthropathy, bilateral hilar adenopathy. HEERFORDT SYNDROME (uveoparotid fever): uveitis, parotitis, fever and facial nerve palsy. MIKULICZ SYNDROME: sarcoidosis plus lacrimal gland involvement. VOGT- KOYANAGI-HARADA SYNDROME VKH syndrome is an uncommon multisystem disease of presumed autoimmune etiology. VKH starts with prodromal stage of flulike symptoms. VKH UVEITIS is marked by bilateral granulommatous anterior uveitis, vitritis, choroiditis, optic disc edema and serous retinal detachment. NON OCULAR SIGNS of VKH SYNDROME Acute disease manifests as flulike symptoms with orbital pain, headache, meningismus, dysacusia, tinnitus, fever, photophobia and rarely cranial neuropathies, hemiparesis, transverse myelitis associated with CSF lymphocytic pleocytosis. Chronic stage is marked by resolution of retinal detachment, fundus depigmentation, perilimbal vitiligo (sugiura sign), alopecia, vitiligo and poliosis. SYMPATHETIC OPHTHALMIA SO is a rare diffuse bilateral granulomatous uveitis that may develop after a surgical or accidental trauma to one eye( the exciting eye), followed after a latent period by the appearance of uveitis in the uninjured fellow eye(sympathizing eye). Until recently, accidental penetrating ocular trauma was the most common cause but ocular surgery particularly vitreoretinal surgey has now emerged as the main risk factor. SYMPATHETIC OPHTHALMIA Severe anterior granulomatous uveitis with mutton-fat KPs, posterior synechia, elevation of IOP may be seen. Posterior segment uveitis presents with vitritis, yellowish white choroidal lesions (DALENFUCHS nodules) and exudative RD. Structural complications include cataract,CME, choroidal neovascularization and optic atrophy. SYMPATHETIC OPHTHALMIA History of trauma helps differentiate SO from other diseases with granulomatous uveitis and uveitis starts and is more severe in the exciting eye. The precise etiology of SO is unknown and in majority of patients there is a history of penetrating ocular trauma complicated by incarceration of the uveal tissue. BEHCET DISEASE A chronic, relapsing, occlusive systemic vasculitis of unknown etiology that is characterized by a uveitis that can affect the anterior and posterior segments of the eye, often simultaneously. The typical age of onset is between 25 and 35 years, but can al o develop as early as 10-15. NONOCULAR BEHCET ORAL. DERMATOLOGIC. GENITAL ULCERS. SYSTEMIC VASCULITIS. NEUROLOGIC Oral manifestations of BEHCET DISEASE Oral aphthae are the most frequent finding in Behcet disease.These are recurrent mucosal ulcers of the lips, gums, palate, pharynx and tongue that produce significant discomfort and pain. They are discrete, round or oval, white ulcerations with red rims. Genital ulcers are quite similar to oral lesions. BEHCET DISEASE Gastrointestinal involvement occurs as ulcers of the esoghagus, stomach and intestines. Pulmonary disease manifests as pulmonary arteritis with aneurysms. Arthritis occurs 50% of cases, the knee is most affected. NEUROLOGIC BEHCET CNS vasculitis is the most serious manifestation of BEHCET and occurs in 10% of cases. CNS BEHCET creates headache, strokes, palsies and confusional states. Cranial nerve palsies, papillitis and papilledema are sometimes seen. OCULAR BEHCET Anterior uveitis is nongranulomatous with transient hypopyon. Posterior uveitis is a sight threatening necrotizing retinal vasculitis. Branch retinal artery and vein occlusion, vitritis and CME may be seen. Retinitis as retinal infiltrates and optic neuropathy as optic papillitis leading to optic atrophy may be seen. MANAGEMENT OF UVEITIS THE FIRST STEP IN THE MANAGEMENT OF UVEITIS IS TO DETERMINE WHETHER UVEITIS IS INFECTIOUS OR NONINFECTIOUS ( AUTOIMMUNE ) AND IS SIGHT THREATENING OR NOT ANY MISTAKE IN THIS APPROACH IS NOT FORGIVEABLE AND COULD BE DISASTEROUS TO THE FINAL VISUAL PROGNOSIS. UVEITIS THERAPY MOST PATIENTS WITH ACTIVE UVEITIS AND ALL THOSE WITH ACUTE ANTRIOR UVEITIS REQUIRE TREATMENT. TREATMENT IS NOT RECOMMENDED FOR SOME FORMS OF UVEITIS IF THE INFLAMMATION IS NEIGHTER PROGRESSIVE NOR SIGHT THREATENING. UVEITIS THERAPY THE GOAL OF TREATMENT OF UVEITIS IS RAPID RESOLUTION OF OCULAR INFLAMMATION, PREVENTION OF SEQUELAE FORMATION AND RESTORATION OF VISION. DIAGNOSIS OF PROBABLE UNDERLYING DISEASE NOT ONLY DIRECTS THE PHYSICIAN TO START PROPER TREATMENT BUT ALSO PREVENTS FURTURE RECURRENCES THAT COULD BE SIGHT THREATENING WITH EACH ATTACK. UVEITIS THERAPY TREATMENT IS CURRENTLY BASED ON BOTH EVIDENCE AND PROTOCOLS AND ALSO BY EXPERIENCE OF THE PHYSICIAN OR THE OPHTHALMOLOGY CENTER INVOLVED IN UVEITIS MANAGEMENT IN AUTOIMMUNE UVEITIS, IT IS NOT ALWAYS A RULE TO WAIT FOR ACHIEVEMENT OF SPECIFIC DIAGNOSIS AS UNJUSTIFIED DELAY IN TREATMENT MAY SOMETIMES CREATE IRREPARABLE DAMAGE TO THE OCULAR STRUCTURES AND PERMANENT VISION LOSS. UVEITIS THERAPY TREATMENT OF AUTOIMMUNE UVEITIS CONSTITUTES THE FOLLOWING APPROACHES : MEDICAL : CORTICOSTEROIDS . IMMUNOSUPPRESSIVES. BIOLOGIC AGENTS. OCULAR SURGERY : CATARACT SURGERY GLAUCOMA SURGEY VITREORETINAL SURGERY. CORTICOSTEROID IT SHOULD BE EMPHESIZED THAT STEROIDS ARE THE MAINSTAY OF THERAPY PARTICULARLY WHEN UVEITIS IS ASSOCIATED WITH SYSTEMIC DISEASE IN INFECTIOUS UVEITIS STEROIDS USE IN COMBINATION WITH SPECIFIC ANTIMICROBIAL THERAPY MAY REDUCE THE INFLAMMATORY RESPONSE AND THE ACCOMPANYING TISSUE DAMAGE IF NECESSARY AND BASED ON CLINICAL JUDGEMENT , IN INFECTIOUS UVEITIS SYSTEMIC STEROIDS SHOULD BE STARTED 48 HOURS AFTER COMMENCEMENT OF ANTIMICROBIAL THERAP DISCONTINUATION OF STEROIDS SHOULD BE MADE 7 DAYS BEFORE ANTIMICROBIAL THERAPY IS TERMINATED IMMUNOMODULATION ALKYLATING AGENTS : CHLORAMBUCIL, CYCLOPHOSPHAMIDE. ANTIMETABOLITES: AZATHIOPRINE, METHOTREXATE, MYCOPHENOLATE MOFETIL T CELL INHIBITORS: CYCLOSPORINE, FK-506 (TACROLIMUS ) COMPLICATIONS : MYELOSUPPRESSION, NEPHROPATHY, HEPATOTOXICITY, SUPERINFECTION, GI UPSET, MALIGNANCY. GONADAL ATROPHY IMMUNOMODULATION UNLIKE SYSTEMIC STEROIDS , CONTROL OF INFLAMMATION IS NOT ACHIEVED BY THE APPLICATION OF IMMUNOSUPPRESSIVES IN INFECTIOUS UVEITIS, SO IMMUNOSUPPRESSIVES ARE ABSOLUTELY CONTRAINDICATED IN INFECTIOUS UVEITIS AND THEIR USE LEADS TO DETERIORATION AND POGRESSION OF THE INFECTIOUS PROCESS. BIOLOGIC AGENTS TUMOR NECROSIS FACTOR INHIBITORS: INFLIXIMAB ( REMICADE ) IS THE FIRST DRUG, I.V ROUTE IS USED. VERY EFFECTIVE ETANERCEPT( ENBREL ) : SUBCUTANEOUS ROUTE, LESS EFFECTIVE. ADALIMUMAB( HUMIRA ), SUBCUTANEOUS ROUTE WITH PROMISING RESULTS. CETROLIZUMAB PEGOL( CIMZIA ): IS THE NEWEST DRUG IN THIS GROUP WITH SUBCUTANEOUS ROUTE BUT NO PUBLISHED DATA ARE AVAILABLE ON ITS EFFECTIVENESS IN UVEITIS. ROUTES OF DRUG ADMINISTRATION IN UVEITIS TOPICAL TREATMENT FOR ANTERIOR UVEITIS: DROPS , OINTMENTS SYSTEMIC ADMINISTRATION: PARTICULARLY WHEN UVEITIS IS ASSOCIATED WITH SYSTEMIC DISEASE PERIOCULAR INJECTIONS: TRIAMCINOLONE INTRAVITREAL INJECTIONS: TRIAMCINOLONE, DEXAMETHASONE, METHOTREXATE, ANTI- VEGFS INTRAVITREAL IMPLANTS: FLUOCINOLONE ACETONIDE ( RETISERT), DEXAMETHASONE (OZURDEX ). DEXAMETHAZONE IMPLANT MAY BE LONGER LASTING THAN TRIAMCINOLONE . PITFALLS OF INTRAVITREAL INJECTIONS & IMPLANTS FLUOCINOLONE ACETONIDE ( RETISERT ) IMPLANT RELEASES THE DRUG OVER A PERIOD OF 30 MONTHS BUT IN CONTRAST TO OZURDEX REQUIRES SURGICAL PLACEMENT. EXPERIENCE IS LIMITED OVER THE APPLICATION OF INTRAOCULAR BIOLOGIC AGENTS AND THEIR USE IS NOT CURRENTLY PROMISING PITFALLS IN INTRAVITREAL DRUG THERAPY INTRAVITREAL METHOTREXATE REDUCES INFLAMMATION, VITREITIS AND MACULAR EDEMA WITHOUT RISING IOP IN PATIENTS WITH A HISTORY OF STEROID RESPONSE. UVEITIS THERAPY SIMILAR TO METHOTREXATE, ANTI- VEGF AGENTS HAVE THE ADVANTAGE OVER TRIAMCINOLONE ACETONIDE OF BEING MUCH LESS LIKELY TO CAUSE CATARACT PROGRESSION OR A RISE IN IOP HOWEVER ANTI-VEGF AGENTS HAVE LESS ANTIINFLAMMATORY EFFECT MAKING THEM LESS SUITABLE FOR THE TREATMENT OF CME IN UVEITIS. SYSTEMIC STEROID PITFALLS DIABETES MELLITUS. OSTEOPOROSIS. HYPERTENSION. MENTAL DISORDER INCREASE IN BODY WEIGHT CUSHINGOID APPEARANCE INTRAVITREAL INJECTION PITFALLS CATARACT FORMATION GLAUCOMA ENDOPHTHALMITIS RETINAL DETACHMENT NEED FOR REPEATED INJECTIONS INTRAVITREAL IMPLANT PITFALLS CATARACT FORMATION. IOP RISE. HYPOTONY. IMPLANT MULFUNCTION. RETINAL DETACHMENT. ENDOPHTHALMITIS. SCLERAL THINNING. GLOBE PERFORATION OPPORTUNISTIC INFECTIONS: CMV AND HERPETIC RETINITIS INFECTIOUS UVEITIS TOXOPLASMOSIS: THE MOST COMMON ETIOLOGY OF INFECTIOUS UVEITIS IN ALL AGE GROUPS, SELF LIMITED IN IMMUNOCOMPETENT INDIVIDUALS. STANDARD RX: PYRIMETHAMINE + SULFADIAZINE. CLINDAMYCIN IS AN OPTION. AZITHROMYCIN. TOXOPLASMOSIS SULFAMETHOXAZOLE + TRIMETHOPRIM IS AN OPTION TO STANDARD RX. ORAL STEROIDS CAN BE ADDED 2 DAYS AFTER SYSTEMIC THERAPY IF OCULAR INFLAMMATION IS SEVERE AND DESTRUCTIVE. OCULAR TOXOCARIASIS PERIOCULAR AND SYSTEMIC STEROIDS ARE EFFECTIVE IN OCULAR TOXOCARIASIS. ANTIHELMINTHIC AGENTS LIKE THIABENDAZOLE, ALBENDAZOLE AND MEBENDAZOLE ARE HELPFUL IN SYSTEMIC TOXOCARIASIS BUT MAY WORSEN OCULAR INFLAMMATION. SYPHILIS OCULAR SYPHILIS CAN OCCUR DURING ANY STAGE OF DISEASE AND CAN AFFECT ALL STRUCTURES OF THE EYE : PARETERAL PENICILLIN G IS THE DRUG OF CHOICE IN THE TREATMENT OF ALL STAGES OF SYPHILIS. JARISCH-HERXHEIMER REACTION SOMETIMES DEVELOPS DURING TREATMENT AND IS MANIFESTED AS : MALAISE, FEVER, SWEATING, ANXIETY AND TEMPORARY EXACERBATION OF SYPHLITIC LESIONS: THE MECHANISM NOT UNDERSTOOD ACUTE RETINAL NECROSIS ( ARN) ARN TYPICALLY CAUSED BY HERPES SIMPLEX VIRUS 1, 2 AND VARICELLA ZOSTER VIRUS : TREATMENT : I.V ACYCLOVIR, ORAL VALACYCLOVIR, ORAL FAMCYCLOVIR. INTRAVITREAL GANCYCLOVIR. INTRAVITREAL FOSCARNET. ARN SYSTEMIC CORTICOSTEROIDS ARE TYPICALLY USED AFTER ANTIVIRAL TREATMENT TO HELP DECREASE INFLAMMATION: PROPHYLACTIC LASER PHOTOCOAGULATION TO THE BORDER OF NECROTIC RETINA IS CONTROVERCIAL AND HAS BEEN ADVOCATED TO REDUCE THE RISK OF RETINAL DETACHMENT. ARN RETINAL DETACHMENT OFTEN REQUIRES VITRECTOMY AND SILICONE INJECTION. LOW VISION IS DUE TO RETINAL DETACHMENT OR OPTIC NERVE INVOLVEMENT CMV RETINITIS CMV IS A HERPES VIRAL INFECTION IN IMMUNOCOMPROMISED PATIENTS. PARENTERAL THERAPY WITH GANCYCLOVIR OR FOSCARNET. ORAL VALACYCLOVIR EQUALLY EFFECTIVE TO I.V THERAPY. INTRAVITREAL GANCYCLOVIR 2mg AND FOSCARNET 2.4 mg. GANCYCLOVIR INTRVITREAL IMPLANT. DIFFUSE UNILATERAL SUBACUTE NEURETINITIS ( DUSN ) CAUSED BY ANCYLOSTOMA CANIUM AND BAILISACARIS PROCYONIS. TREATMENT BY ANTIHELMINTHIC AGENTS: ALBENDAZOLE AND THIABENDAZOLE. DIRECT LASER PHOTOCOAGULATION OF THE INTRARETINAL PARASITE. LYME DISEASE MULTISYSTEM INFECTIOUS DISEASE CAUSED BY SPIROCHETE ( BORRELIA BURGDORFERI ). IT IS TRANSMITTED TO HUMANS BY TICK: IXODES SCAPULARIS AND IXODES PACIFICUS. ORAL ANTIBIOTIC AT EARLY STAGE I.V ANTIBIOTICS IN LATER STAGES: CEFTRIAXONE, PENICILLIN, TETRACYCLINE, DOXYCYCLINE, ERYTHROMYCIN. TUBERCULOSIS INTRAOCULAR T.B CAN PRESENT AS ACUTE OR CHRONIC GRANULOMATOUS UVEITIS. IZONIAZID, RIFAMPIN, PYRAZINAMIDE FOR 6-9 MONTHS. ETHANBUTOL OR STREPTOMYCIN CAN BE ADDED IN CASE OF DRUG RESISTANCE. ORAL STEROIDS REDUCE THE INFLAMMATORY COMPONENT OF T.B. BRUCELLOSIS DOXYCYCLINE AND RIFAMPIN. DOXYCYCLINE AND STREPTOMYCIN. IN CHILDREN RIFAMPIN AND TRIMETHOPRIM +SULFAMETHOXAZOLE