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Educational Workshop EW08: Management of Ocular Parasitic Diseases

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Educational Workshop EW08: Management of Ocular Parasitic Diseases Educational Workshop EW08: Management of ocular parasitic diseases Arranged with the ESCMID Study Group for Clinical Parasitology (ESGCP) Convenors: Birgitta Evenbard (Umea, SE) Carmen-Michaela Cretu (Bucharest, RO) Faculty: Francisco Arnalich (Madrid, Spain) Carmen-Michaela Cretu (Bucharest, Romania) Hélène Yera (Paris, France) Peter Chiodini (London, United Kingdom) - no handout available 1 2 Arnalich - Ocular acanthamoebiasis Ocular Acanthamoebiasis Dr. FRANCISCO ARNALICH CORNEA UNIT- OPHTHALMOLOGY SERVICE HOSPITAL UNIVERSITARIO RAMÓN Y CAJAL DE MADRID, SPAIN “WITHOUT CLINICAL AWARENESS AND THEREFORE PROMPT DIAGNOSIS AND TREATMENT IT CAUSES BLINDNESS” • Mainly a primary corneal disease which can extend to: • Sclera • Anterior chamber • Iris • Vitreous chamber • Retina 3 Arnalich - Ocular acanthamoebiasis • Contact Lens (CL) Wearer • Poor CL hygiene • Immune-competent THE CANDIDATE • ACANTHAMOEBA • HARTMANELLA • NAEGLERIA • VAHLKAMPFIA ETHIOLOGY • ACANTHAMOEBA (genotypes T1-18) • T2, T3, T4, T5, T6, T10, T11 y T15 • T4 Causes 100%-85% of ocular acanthamoebiasis • In our case series in the last 5 years: T4 T3 T11 ETHIOLOGY 4 Arnalich - Ocular acanthamoebiasis ETHIOLOGY ETHIOLOGY TROPHOZOITE CYST LIFE CYCLE 5 Arnalich - Ocular acanthamoebiasis • Incidence 1-8% Microbial keratitis • CONTACT LENS WEARER (85%) • Soft contact lens • Orthokeratology • Multiuse solutions • Bath or use of contaminated waters/well water • NON CONTACT LENS WEARER (3-15%) • Trauma associated with contaminated waters • Surgical trauma • Use of well water and unnoticed corneal trauma EPIDEMIOLOGY- RISK FACTORS • Traumatic event related with water or contaminated soils • Contact lens wearer with poor hygienic care • Poor response to conventional antibacterial treatment • Disproportionate Pain CLINICAL SIGNS OF AWARENESS CLINICAL MANIFESTATIONS 6 Arnalich - Ocular acanthamoebiasis EPITHELIOPATHY EARLY CLINICAL MANIFESTATIONS EPITHELIOPATHY EARLY CLINICAL MANIFESTATIONS PERINEURAL INFILTRATES (Almost Pathognomonic) EARLY CLINICAL MANIFESTATIONS 7 Arnalich - Ocular acanthamoebiasis LIMBITIS EARLY CLINICAL MANIFESTATIONS CORNEAL ULCERATION LATE CLINICAL MANIFESTATIONS RING INFILTRATE LATE CLINICAL MANIFESTATIONS 8 Arnalich - Ocular acanthamoebiasis CORNEAL ABSCESS AND PERFORATION LATE CLINICAL MANIFESTATIONS IRIS ATROPHY EXTRACORNEAL MANIFESTATIONS- INFLAMATORY CATARACT EXTRACORNEAL MANIFESTATIONS- INFLAMATORY 9 Arnalich - Ocular acanthamoebiasis SCLERITIS EXTRACORNEAL MANIFESTATIONS- INFLAMATORY POSTERIOR SEGMENT ISCHEMIC INFLAMMATORY SYNDROME EXTRACORNEAL MANIFESTATIONS- INFLAMATORY INTRAOCULAR INFECTION EXTRACORNEAL MANIFESTATIONS- INFECTIOUS 10 Arnalich - Ocular acanthamoebiasis SCLERITIS EXTRACORNEAL MANIFESTATIONS- INFECTIOUS CLINICAL AWARENESS: CL, PAIN, NOT RESPONSIVE DIAGNOSIS SLIT LAMP EXAMINATION DIAGNOSIS 11 Arnalich - Ocular acanthamoebiasis IN VIVO CONFOCAL MICROSCOPY DIAGNOSIS • IN VIVO CONFOCAL MICROSCOPY DIAGNOSIS • IN VIVO CONFOCAL MICROSCOPY DIAGNOSIS 12 Arnalich - Ocular acanthamoebiasis • IN VIVO CONFOCAL MICROSCOPY • Sensitivity 50% • Specificity 65.8-81.6% • DO NOT RELY ON CONFOCAL FOR DIAGNOSIS IF THE RESPONSE TO THERAPY IS POOR DIAGNOSIS CORNEAL SCRAPE ( Include epithelium or stroma with a 27-30G needle) FOR: Smears Cultures in non nutrient Agar PCR DIAGNOSIS CORNEAL BIOPSY DIAGNOSIS 13 Arnalich - Ocular acanthamoebiasis • Must be CYSTICIDAL • Effective if definitive treatment is started within 3-4 weeks from onset TREATMENT Minimum cysticidal concentration in ug/ml PHMB CHX 600 Propamidine 500 Neomycin Paromomycin 400 Polymyxin 300 Ketoconazole Fluconazole 200 Pentamidine 100 Sepazonium 0 Miconazole For 100% kill Clotrimazole No role for topical amino-glycosides or azoles (except voriconazole) TREATMENT POTENTIAL NEW THERAPIES • Voriconazol (oral, intraocular, and topical) • UV Cross-linking treatment • Statins TREATMENT 14 Arnalich - Ocular acanthamoebiasis DRUG ADMINISTRATION • Hourly day and night for 2 days • Hourly day only for 3 days • Then reduce to 6x daily taper to 4x Drug toxicity common! TREATMENT CONTROLLING CORNEAL INFLAMMATION • Role of topical steroids- for deteriorating inflammation & pain • Defer for 2 weeks after started treatment • Only use with biguanides • Continue biguanides for 4 weeks after steroids are discontinued TREATMENT TREATMENT 15 Arnalich - Ocular acanthamoebiasis TREATMENT OF PERSISTENTLY CULTURE POSITIVE KERATITIS • Switch diamidines and biguanides • Increase concentration of eye drops • PHMB 0.06% or Clorhexidine 0.2% • Add oral Voriconazole • Cryotherapy (for infective scleritis) • Corneal graft • Recurrence common • Large diameter keratoplasty TREATMENT TREATMENT • DELAY ON DIAGNOSIS (>3 WEEKS) • STAGE 3 AT PRESENTATION • OLDER AGE • NON T4 KERATITIS PROGNOSIS 16 Arnalich - Ocular acanthamoebiasis • University Institute of Tropical Diseases and Public Health fo the Canary Islands, University of la Laguna • Basilio Valladares • Jacob Lorenzo Morales • José Piñeiro • Carmen Martin-Navarro • Tropical Disease Unit of Hospital Universitario Ramón y Cajal Madrid, Spain • Rogelio López Vélez ACKNOWLEDGMENT 17 Cretu - Ocular larva migrans, cysticercosis, dirofilariasis CARMEN MICHAELA CRETU University of Medicine and Pharmacy “Carol Davila” Colentina Clinical Hospital – Parasitology Department Bucharest OCULAR LARVA MIGRANS CYSTICERCOSIS DIROFILARIASIS CLINICAL CASE . 38 years old, male patient, worker . Medical history: Type II Diabetes, no insulin required . February 2011: R E Total uveitis, possible ocular toxocariasis Secondary glaucoma RE progressive decrease of vision, up to perception of fingers’ movements, headache ‐ Biomicroscopic ex: Perikeratic congestion, epithelial corneal edema, iris hemorrhages and neovascular membrane → scars of the iris ‐ leuchocoria ‐ Fundus ex: difficult examination, hazy, inflammation of posterior vitreous, prominent papilla and papillary edema, retinal hemorrhages, narrow arteries and dilated veins ‐ Ocular pressure: 60 mmHg LE normal ‐ Orbit X‐ray: normal, no eyeball foreign bodies ‐ US: RE hyper echoic vitreal areas, temporal retinal folds ‐ retinal detachment ‐ IRM head and orbit :REposterior, external and lateral inflammation, retinal folds and retinal detachment; maxillary sinusitis; ocular tumor is excluded ‐ Laboratory: hiperleucocytosis (11000/cmm), no Eo; liver and kidney normal function; blood glucose 144 mg/dl Inflammatory syndrome present (ESR 25/45 mm/h; FH 640 mg/ml) Toxocara IgG serology (ELISA) – positive Toxoplasma, CMV, Leptospira, Brucella serology ‐ negative 18 Cretu - Ocular larva migrans, cysticercosis, dirofilariasis RE LE 28.03.2011 RE 28.03.2011 28.03.2011 Treatment: corticosteroids, diuretics, anti‐diabetics Referred to Infectious Diseases Department –Increased dosage of corticosteroids and Albendazole 800mg/day, for 10 days –worsened Referred to Ophthalmology and Parasitology Dept in Bucharest March 2011: RE Ocular pressure 44mm HG Fundus ex: vitreal inflammation, retinal folds, macular edema, retinal granuloma Toxocara avidity –AI 0.46 (recent infection, less than 20 weeks) Treatment: progressively decreased corticosteroids plus Diethylcarbamazine May 2011: RE Fundus ex: ‐ Vitreal inflammation, retinal folds, macular edema, retinal granuloma ‐ Central Retinal Vein Thrombosis Toxocara serology ‐ positive November 2011: RE disorganized Fundus ex: Total optic nerve atrophy Central Retinal Vein Thrombosis SEQUELS Vitreous precipitates RE RE RERE 28.03.2011 28.03.2011 28.03.2011 RE RE 18.05.2011 18.05.2011 19 Cretu - Ocular larva migrans, cysticercosis, dirofilariasis IMAGING DIAGNOSIS Ocular MRI –retinal detachment Ocular US –vitreal reaction, retinal folds LARVA MIGRANS SYNDROME LM Syndrome –migration of some nematode larvae, through the tissues of parathenic host, after invading the host either by digestive (ingestion of infective eggs) or subcutaneous penetration of the larvae. (Schantz and Michelson, 1992) LMV est une migration prolongée et la longue persistance des larves du parasite, habituellement un nématode, dans les organes internes d’une hôte anormale (paratenique). (Petithory et al., 1994) VLM - Toxocara canis - Spirometra spp. - Toxocara catii Etiology - Toxocara vitulorum - Balysascaris spp. - Parascaris equorum - Gnathostoma spp. - Ascaris suum LIFE CYCLE Toxocara canis adults (Cretu & Mihailescu ) Toxocara spp. eggs (Cretu & Mihailescu) Eggs need soil development The disease is due to the larval stage in human tissues During the migratory stage, larvae are trapped in tissue granulomas The life cycle remains unaccomplished, larvae wondering and remaining in the tissues The pathology is due to the antigenic stimulation produced by the migrating larvae and tissue granuloma reaction ! Congenitally transmission of Toxocara larvae in dogs (puppies ‐ important source of infection) 20 Cretu - Ocular larva migrans, cysticercosis, dirofilariasis TRANSMISSION Accidental ingestion of fertilized egg (vegetables, dirty hands etc…) L T Glickman and J‐F Magnaval, 1993. Zoonotic roundworm infections. Inf Dis Clin North America. 7(3): 717‐731 Consumption of raw chicken liver, cattle meat or rabbit giblets K Nakagura et al: 1989 Toxocariasis possible caused by ingesting raw chicken. J Infect Dis 160: 735‐ 736 D Sturchler et al: 1990 Transmission of toxocariasis. J Infect Dis 571: 572 Espana et al: 1993. Secondary urticaria due to toxocariasis: possibly caused by ingesting raw cattle meat. J Invest Allergol Clin Immunol. 3(1): 51‐52 Y Morimatsu et al. 2006. A familial case of Visceral Larva Migrans after ingestion of raw chicken liver:
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