Blurred vision and floaters. May have redness and photophobia. Pain depends on the severity of associated iridocyclitis.

(See Figure 12.5.1.)

Other

• Anterior: Mild anterior chamber spillover may be present, increased IOP in 10% to 20%.
• Posterior: Vitreous debris, optic disc swelling due to peripapillary lesions often with edema extending into the retina, neuroretinitis with/without macular star, optic neuritis with significant vitritis, retinal vasculitis, rarely retinal artery or vein occlusion in the area of the inflammation. Kyrieleis arteritis is periarterial exudate accumulation, which may occur near the retinitis or elsewhere in the retina; IVFA does not show vascular occlusion. Chorioretinal scars are occasionally found in the uninvolved eye. CME may be present.

NOTE:

Toxoplasmosis is the most common cause of posterior uveitis and accounts for approximately 90% of focal necrotizing retinitis.

Toxoplasmosis can also develop in the deep retina (punctate outer retinal toxoplasmosis) with few to no vitreous cells present. More common in HIV-infected patients. See SPECIAL CONSIDERATION IN IMMUNOCOMPROMISED PATIENTS at the end of this section.

See 12.3, POSTERIOR UVEITIS, for a complete list. The following rarely may closely simulate toxoplasmosis.

• Syphilis (See 12.12, SYPHILIS) and tuberculosis.
• Toxocariasis: Usually affects children. Chorioretinal scars are not typically seen. See 12.3, POSTERIOR UVEITIS and 8.1, LEUKOCORIA.
• ARN. See 12.8, ACUTE RETINAL NECROSIS (see Table 12.8.1).
• PORN. See 12.8, ACUTE RETINAL NECROSIS (see Table 12.8.1).

1. Mild peripheral retinochoroiditis.
   • Self-limited in immunocompetent patients. May consider observation only for peripheral lesions.
   • Treat elevated IOP with antiglaucoma medications and anterior uveitis with topical cycloplegic (e.g., cyclopentolate 1% to 2% t.i.d.) with or without topical steroid (e.g., prednisolone acetate 1% q2h).
2. Treatment usually recommended for lesions in the macula, within 2 to 3 mm of the disc, threatening a large retinal vessel, associated with severe vitritis causing decreased vision, or disease in an immunocompromised patient. Immunocompromised patients may require extended treatment.
   • Classic first-line triple therapy (for 4 to 6 weeks):
     • Pyrimethamine, 200 mg p.o. load (or two 100 mg doses p.o. 12 hours apart), and then 25 to 50 mg p.o. daily. Do not give pyrimethamine to pregnant or breastfeeding women (spiramycin 1 g p.o. t.i.d. for women who seroconvert in pregnancy).
     • Folinic acid 10 mg p.o. every other day (to minimize bone marrow toxicity of pyrimethamine).
     • Sulfadiazine 2 g p.o. load and then 1 g p.o. q.i.d. Expensive and difficult to obtain; trimethoprim/sulfamethoxazole 160 mg/800 mg twice daily may be substituted as described below.
     • Prednisone may be added 20 to 60 mg p.o. daily beginning at least 24 hours after initiating antimicrobial therapy and tapered 10 days before stopping antibiotics. Periocular steroids should not be given.

Systemic steroids should only rarely be used in immunocompromised patients. Before systemic steroid use, evaluation of fasting blood sugar/hemoglobin A1C and studies to rule out tuberculosis are prudent.

NOTE:

Due to potential bone marrow suppression, a CBC must be obtained once per week while a patient is taking pyrimethamine. If the platelet count decreases below 100,000, then reduce the dosage of pyrimethamine and increase the folinic acid. Patients taking pyrimethamine should not take vitamins that contain folic acid. The medication should be given with meals to reduce anorexia.

• Alternate regimens:
  • Clindamycin 150 to 450 mg p.o. t.i.d. to q.i.d. (maximum 1.8 g/d) may be used alone, with pyrimethamine as the alternative therapy (if the patient is sulfa allergic), or as an adjunct (quadruple therapy). Patients on clindamycin should be warned about pseudomembranous colitis, and the medication should be stopped if diarrhea develops. Intravitreal injection of clindamycin (0.1 mg/0.1 mL) can be effective for macular-threatening cases, or when the patient is intolerant to systemic medication. Combined intravitreal clindamycin (0.1 mg/0.1 mL) and dexamethasone (0.4 mg/0.1 mL) have been reported helpful.
  • Atovaquone 750 mg p.o. q.i.d., used as an alternative similar to clindamycin.
  • Trimethoprim/sulfamethoxazole (160 mg/800 mg) one tablet p.o. b.i.d., with or without clindamycin and prednisone.
  • Azithromycin loading dose 1 g (day 1) and then 250 to 500 mg daily. May be used alone or in combination with pyrimethamine (50 mg daily).
  • Spiramycin 400 mg p.o. t.i.d. may be considered in cases of pregnancy, but must be obtained from CDC.
  • Anterior segment inflammation is treated as above.

• 3.Vitrectomy has been used for nonclearing dense vitritis or other complications.
• 4.Maintenance therapy (if the patient is immunosuppressed)
  • Trimethoprim/sulfamethoxazole 160 mg/800 mg one tablet p.o. three times a week.
• or
  • If sulfa-allergic (common in HIV-infected patients), may use clindamycin 300 mg p.o. q.i.d.
• 5.Prophylaxis: In a patient with a history of toxoplasmosis undergoing cataract or refractive surgery, consider using trimethoprim/sulfamethoxazole b.i.d. during the perioperative period.

In 3 to 7 days for blood tests and/or ocular assessment, and then every 1 to 2 weeks on therapy.

Special Consideration in Immunocompromised Patients

Vitritis usually much less prominent. Adjacent retinochoroidal scars may not be present. The lesions may be single or multifocal, discrete or diffuse, and unilateral or bilateral. CNS imaging is essential because of high association with CNS disease (e.g., toxoplasmic encephalopathy in HIV patients). Diagnostic vitrectomy may be necessary because of the multiple simulating entities and the variability of laboratory diagnostic tests. Systemic steroids for ocular toxoplasmosis should be used very cautiously in patients with AIDS.