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