Daraprim

Revisiting Toxoplasmosis.

Whenever I discuss ocular disease, I stress that diagnosing is the difficult part. This month's case, however, shows that treatment can be just as challenging.

THE CASE: In 1994, 1 diagnosed Jewell with ocular toxoplasmosis OS. Her case was self-limiting; she was quickly able to resume comfortable contact lens wear.

Now, 4 1/2 years later, Jewell is 58 years old and has been wearing soft contact lenses for more than 10 years. She now complains of seeing "floating specks" with blurring in one eye. A week earlier, she'd noticed two large spots in front of the left eye. With time, the spots became smaller but more numerous.

When she went to work earlier (on the day I saw her), she had difficulty focusing on the computer, as if a shadow were clouding her vision OS. The eye was irritated and red for the first time, so she called me.

A closer look Jewell took hormone supplements. She also took fexofenadine (Allegra) for chronic allergies. Her vision with monovision soft contact lenses was 20/20 at distance but 20/50 at near. (The left lens was designed to be her near eye.) Her pupils were equal, round and reactive with no afferent pupillary defect. Extraocular muscles showed no restrictions; she had no pain on movement. A refraction yielded 20/20 vision OD but only a hazy 20/40 OS.

When I examined her with the slit lamp, she was normal OD. Her left eye showed 2+ bulbar conjunctival injection nasally and temporally. The anterior chamber was positive for 1+ cell but no flare, and showed no synechia or keratic precipitates. Intraocular pressure (IOP) was 15 mm Hg OD, 25 mm Hg OS.

Dilated fundus examination revealed the reason for Jewell's symptoms. The vitreous was clouded with 2+ vitreal cells centrally. A white retinal lesion appeared through the haze, 2 disk diameters inferonasally to the optic nerve head (see top image). I also saw two old, inactive chorioretinal scars superonasally in the mid-periphery.

Jewell had a severe recurrence of ocular toxoplasmosis involving the retina, vitreous and anterior chamber. It also obscured her vision. Because of the severity and the fact that it was a reactivation, I treated it with 300 mg of oral clindamycin (Cleocin) q.i.d. and 1000 mg of sulfadiazine (Microsulfon) q.i.d. I also prescribed prednisolone 1% (Pred Forte) OS q.i.d. to calm the iritis. The toxoplasmosis titer I sent her for came back dramatically elevated, so I referred her to a retinal specialist. He concurred with my decisions and asked Jewell to continue follow-up with me.

There and back again Ocular toxoplasmosis accounts for 30% to 50% of posterior uveitis cases. Though clinically, it appears that only the anterior layers of the retina are affected, toxoplasmosis is a retinochoroiditis. The deeper lay ers of the retina and the choroid can be involved. The most common characteristic is the focal exudative retinitis lesion. Direct necrosis of retinal tis

sue by Toxoplasma gondii (an intestinal parasite of the cat), causes the retinitis. Humans probably acquire the parasite by eating undercooked meat from cows that ingested cat feces. In the retina, T gondii multiplies and ruptures retinal cells, releasing more organisms that invade new, adjacent retinal tissue. These new sites are the "satellite lesions" characteristic of toxoplasmosis reactivation. A hypersensitivity reaction develops as the body tries to defend itself, causing vitritis and iritis.

Remember these points:

* A toxoplasmosis patient averages 2.7 recurrences throughout her lifetime. Each recurrence is more severe than the last.

* The breakdown of toxoplasma cysts in the retina causes recurrences. Diagnosis is made based on clinical signs, but a positive toxoplasma titer confirms it. The most common differential is toxocariasis, which affects teens and people in their early 20s. Most toxoplasmosis patients are between ages 30 and 50.

Treatment for Jewell

Treatment is unnecessary if vision isn't decreased, even when a vitritis exists. If the patient's uncomfortable from an iritis, recommend topical steroids. Save oral therapy for protracted cases or those that decrease vision

Use oral therapy if the lesions are located peripapillary or perifoveally. Effective ones include combinations of pyrimethamine (Daraprim), clindamycin, sufadiazine and corticosteroids. Pyrimethamine can be toxic to bone marrow, so conduct serial complete blood and platelet counts. I recommend clindamycin in place of pyrimethamine (you may need to continue oral therapy for 1 month). A subTenon's injection of a corticosteroid is indicated for cases recalcitrant to oral therapy. The longer active toxoplasmosis persists, the greater the chance of cystoid macular edema or even choroidal neovascular membrane formation.

Because no treatment has direct action on the parasite, toxoplasmosis is incurable. Treatment only controls the inflammation. Jewell's rocky road I monitored Jewell every week for 2 months, but the inflammation persisted. Her visual acuity (VA) dropped to 20/200 OS, and I worried that macular edema had developed. However, an intravenous fluorescein angiogram ruled that out (see bottom figure, page 115). The retinal specialist recommended a steroid. We chose a sub-Tenon's injection of triamcinolone (Kenalog), which was administered 1 week later. Jewell kept taking clindamycin and sulfadiazine.

Jewell improved after the injection. A month later, the retinal specialist discontinued oral therapy. Two months after steroid treatment, Jewell's VA had improved to 20/40 OS. Now, 8 months after the recurrence, Jewell is wearing contact lenses again and seeing 20/25 OS. If she has another recurrence, I'll be more aggressive and quicker, with treatment. OM

CLINICAL PEARLS *An iritis, which may be granulomatous, often accompanies toxoplasmosis. You should treat it aggressively with a regimen of topical steroids. 1 Increased IOP may sometimes appear. Treat it with a topical betablocker, unless contraindicated, if it remains elevated.

*A vitritis is common in toxoplasmosis. Exudation of white blood cells into the vitreous causes the vitreal haze.

*Remember that not all cases of ocular toxoplasmosis need to be treated. Isolated peripheral lesions and cases in which the patient's vision remains good can safely be monitored without putting the patient on oral therapy.

*Clindamycin works well for toxoplasmosis, but it can cause pseudomembranous colitis. Counsel your patient on this potential side effect and discontinue the drug if diarrhea occurs.

*Order a toxoplasmosis titer for all suspected ocular toxoplasmosis cases. A positive result confirms the diagnosis. Only a positive result is necessary; the level of the titer isn't important.

Contributing Editor Eric Schmidt, O.D., is director of the Bladen Eye Center in Elizabethtown, N.C. He can be reached at KENZIEKATE@aol.com.

Copyright Boucher Communications, Inc. May 2000
Provided by ProQuest Information and Learning Company. All rights Reserved