Ocular toxoplasmosis
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Transcript of Ocular toxoplasmosis
Ocular Toxoplasmosis
Dr. Md. Mominul Islam
Fellow (Vitreo-Retina)
Ispahani Islamia Eye Institute And Hospital Dhaka
Bangladesh
IntroductionCommon zoonosisCaused by Toxoplasma GondiiLife threatening disease (newborn and
immnosuprresed patients)Asymptomatic in immuno competent patientCongenital or Acquired Both eye may affected
Epidemiology Represent with posterior uveitis50-85% in Brazil25% in USA Prevalence: (not well determind)0.6-2% in USA10-17.7% in Brazil
TransmissionBeefUndercooked lamb , pork, chickenEnvironment contaminated by feces of
infected cats familyOrgan transplantationBlood transfusionWater
Biology And Life Cycle Obligate , intracellular protozoanBoth sexual and asexual reproductionDefinitive host – Members of cat familyIntermediate host- Hundreds of species
including mammals, birdsHost tissue - Muscle - Retina - Nervous tissue - Body fluid
ContdThree forms
OocyteTrachyzoite
Bradyzoit (tissue cyst)
Genetics
Type- I• Very virulent•Postnatal acquired ocular infection
Type-II •Less virulent•Congenital infection and toxoplasmic encephalitis
Type-III
•Less virulent
Pathogenesis In immunocompetent patients is characterized
histologically by Foci of granulomatous chorioretinal
inflammation Coagulative necrosis of the retina with
sharply demarcated borders Inflammatory changes can be widespread in
the eye and involve choroid, iris, and trabecular meshwork
ContdIn Immunosuppressed Have both tachyzoites and tissue cysts in
areas of retinal necrosis and within retinal pigment epithelial cells.
Parasites can occasionally be found in the iris, choroid, vitreous, and optic nerve
Ocular presentationSymptoms Floaters Blurring or loss of
vision
Sign (The hallmarks)necrotizing
retinochoroiditisSatellite lesion
adjacent to old hyperpigmented scars
Vitreous inflammation Anterior uveitis Retinal vasculitis is
also present (occationally)
ContdNew or
Acute lesion•Intensely white•Focal lesion overlying vitreous inflammatory haze (head light in the fog)•Acute anterior uveitis
Healed lesion
•Border become more defined•Hyperpigmented after several months•Large scar will have atrophic center (devoid of all choroidal retinal elements)
InvestigationSerological testPCR
Differential DiagnosisInfectious:RubellaCytomegalovirusSyphilisHerpes simplexTuberculosisToxocariasis
ContdNon-infectious:Retinal and choroidal colobomaRetinoblastoma,Retinopathy of prematurityGyrate atrophyRetinal vascular membraneSerpiginous choroidopathy
Outcome And ComplicationCentral vision will be lostPermanent loss of visionSudden loss of vision.
Treatment and PreventionAvailable drugs do not eliminate tissue cysts
and cannot prevent chronic infectionNo treatment has proven to be superior or
even more effective than no treatmentAntitoxoplasmic agents and systemic steroids
have never been studied in large clinical trials
“Classic” therapy:The combination of pyrimethamine,
sulfadiazine, and corticosteroids
Pyrimethamine: 75–100 mg loading dose given over 24 hours, followed by 25–50 mg daily for 4–6 weeks depending on clinical response
Sulfadizine: 2.0–4.0 g loading dose initially, followed by 1.0 g given 4 times daily for 4–6 weeks, depending or clinical response
Prednisone: 40–60 mg daily for 2 to many weeks depending on clinical response; taper off before discontinuing pyrimethamine/sulfadiazine
Folinic acid: 5.0 mg tablet, 2–3 times weekly during pyrimethamine therapy
ContdOther Drugs:Trimethoprim and sulfamethoxazole.Systemic or intraocular clindamycinThe duration of treatment depends on the individual clinical picture Steroid treatment is often administered systemically and always associated with antitoxoplasmic drugs
Local drops are used when anterior uveitis is present
Take Whom Massage Wrong concepts in ocular
toxoplasmosis All cases congenital Must present as a “retinochoroiditis” Vertical transmission (pregnancy) only once in life Cats and meat are the only source No treatment to avoid recurrences All patients need antitoxoplasmic drugs for 4–6 weeks Recurrences are related only to local factors