Ocular Toxoplasmosis

Obligate intracellular protozoan

500 million have antibodies worldwide

50% of adult population in US have asymptomatic infection

28-55% of all cases of posterior uveitis

First isolated from the brain of a “gondii” (North African Rodent)

Cat family is definitive host, can infect other mammals and birds

Oocysts found in intestinal tracts of cats

Cysts ingested (most likely)

Poor hygiene, infected pork, chicken but probably not beef

Can survive outside host for up to 1 year

Two forms in humans: cysts or tachyzoites.

Propensity for cardiac and skeletal muscle and neural tissue (brain & eye)

Most cases are presumed reactivation of congenital infection

2 to 6/1000 women acquire infection while pregnant, 40% risk of transmission to fetus.

Of infected infants: 70% chorioretinal scars, 5% will die or severe disability, 1-2% severe visual impairment

Northern Brazil has high rate of acquired disease

90% lympadenopathy

fever, malaise, occasional sore throat

immunocompromised- fulminant CNS disease

Keratic Precipitates, anterior chamber cell and flare, posterior synechia, cataract

Retinochoroiditis

Vitritis- concentrated over lesion, scaffolding of vitreous strands

Macular edema

Retinal vasculitis

VF defect in area of scar

FFA of active lesion- early blockage and subsequent leakage

In early infection: gray-white fine punctate lesions in deep retina and RPE, progress to more classic lesions

Papillitis, vitreal inflammation, nerve fiber bundle defects

Bullous like inflammatory lesions in mid-periphery

Wide ring-like lesion near extreme periphery resembling pars planitis

Scleritis

Vitreal inflammation causing clouding

Lesion in posterior pole with edema affecting fovea

Lesion in fovea

Subsequent CNVM

Typical lesions

Immunoflourescence, ELISA

Western blot for Toxo antigens

PCR and Southern Blot for Toxo DNA

Angiography: flourescein tagged Ab (successful in rabbit studies)

No truly randomized, controlled clinical trials to compare efficacy

Generally 4-6 weeks, multi-drug regimens

Sulfadiazine 1g PO QID

Clindamycin 150-300mg PO TID-QID (?reduces recurrence, risk of pseudomembranous colitis)

Trimethoprim-sulfamethoxazole (DS) I PO BID

Atovaquone (Mepron) 750mg PO BID (kills cysts in vitro)

Tetracycline 2g load and 250mg PO QID (to replace clindamycin)

Prednisone 20-60 mg/day not used alone

Pyrimethamine, Sulfadiazine, Folinic Acid, Prednisone

Best at reducing size of lesions (49%),

more medication side effects (26%),

recurrence rate at 3 years (42%)

Clindamycin, Sulfadiazine, Prednisone

Reducing size of lesions >1/2 DD (28%)

med side effects (17%)

recurrence rate at 3 years (67%)

Co-trimoxazole, Prednisone

Reducing size of lesions >1/2 DD (11%)

med side effec!ts (4%)

recurrence rate at 3 years (40%)

No treatment (peripheral lesions)

Reducing size of lesions >1/2 DD (20%)

no med side effects

recurrence rate at 3 years (53%)

Recurrence rates not statistically significant

Size of retinal lesion correlated with duration of inflammation

All side-effects were reversible

Delay in starting medication (even up to 1 week) did not alter duration of inflammation

Sub-tenon's steroid- risk of increasing activity of organism

Vitrectomy- for vitreal haze reducing vision, perioperative antibiotics advocated

Cryotherapy and Laser photocoagulation generally not successful