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  • Management of Ocular Toxoplasmosis

    Comprehensive Ophthalmology, Uveitis
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    Introduction

    Ocular toxoplasmosis is caused by the parasite Toxoplasma gondii. The organism may lead to acute or chronic infection in humans. Humans may acquire the disease by ingestion of the cyst of the parasite in undercooked beef, lamb, pork, or chicken. Other modes of transmission include the ingestion or inhalation of oocysts, by organ transplantation from infected donors, or by transplacental transmission. The systemic illness presents as a flu-like illness with fever, postauricular lymphadenopathy, myalgia, and malaise. Following acute systemic illness, the retina and choroid may become infected by the parasite several weeks to several years after the initial systemic illness.

    The most common ocular manifestation is toxoplasmic retinochoroiditis.1 The inner layers of the retina are commonly involved, leading to a focus of necrotizing retinitis with subjacent choroiditis and cells in the vitreous. Retinal vasculitis is common in patients with ocular toxoplasmosis. The lesion may remain active for several weeks, undergoes healing, and forms a pigmented scar in the retina, which may be punched out.1 The retinochoroiditic scar of toxoplasma may harbor the toxoplasma cyst, and the organism may stay viable in the tissue for many years. Rupture of the cyst may lead to the release of toxoplasma organisms and recurrence of retinochoroiditis. Most of the recurrences occur in the second and third decades of life in immunocompetent individuals, and may be triggered by stress or other factors. In immunocompromised patients, eg, patients with AIDS, toxoplasmic retinochoroiditis may be severe, leading to wide destruction of the retina and choroid.

    Therapy

    The major objectives of therapy of toxoplasmosis include:

    • Alleviate the symptoms and signs
    • Control the infectious process
    • Prevent damage by the inflammatory process
    • Prevent recurrences
    • Rehabilitate the vision

    Treatment of acute toxoplasmic retinochoroiditis consists of 2 parts:

    • Treat the acute disease process
    • Manage the sequelae and the complications of ocular toxoplasmosis such as vitreous opacities, cataract, glaucoma, and choroidal neovascular membranes

    Alleviation of Symptoms and Signs

    Patients with ocular toxoplasmosis may present with history of blurring of vision and seeing floaters. In addition, patients may complain of redness and pain. The anterior uveitis may be treated with topical prednisolone acetate 1% eyedrops 4 times daily. Secondary glaucoma is treated with beta blockers such as timolol maleate 0.5% eyedrops twice daily. In some cases, patients may require the addition of carbonic anhydrase inhibitors topically or systemically. Patients with significant fibrin in the anterior chamber may need short-acting cycloplegic/ mydriatic such as cyclopentolate 1.0% eyedrops once every 12 hours.

    Control of the Ocular Infection

    Antimicrobial agents that are used for the inhibition of the tachyzoites of the T. gondii have limited effects against the encysted form of the parasite. Single-drug antimicrobial therapy is not sufficient for the treatment of toxoplasmosis. It is therefore conceded that antimicrobial agents should be combined in the management of toxoplasmosis2-4 (Figure 1 and Figure 2). The antitoxoplasma regimens that are used for the treatment of ocular toxoplasmosis are shown in Table 1.

    Tabbara 2008 Quarter 3
    Figure 1. A 38-year-old male with acquired toxoplasmic retinochoroiditis (A) before and (B) after treatment with oral azithromycin and trimethoprim/sulfamethoxazole.

    tabbara 2008 Quarter 3
    Figure 2. A 50-year-old male with macular toxoplasmic retinochoroiditis (A) before and (B) after therapy with azithromycin and trimethoprim/sulfamethoxazole and systemic steroids.

    tabbara 2008 quarter 3
    Table 1. Guidelines for the Treatment of Ocular Toxoplasmosis.

    Acute toxoplasmic retinochoroiditis is treated with combination of pyrimethamine and sulfonamides. Adult patients with ocular toxoplasmosis are given pyrimethamine 200 mg orally once on the first day, followed by 50 mg orally per day thereafter for a period of 4 weeks. The treatment should be combined with sulfonamides such as sulfadiazine. Sulfadiazine is given at a dosage level of 2 g orally as a loading dose, followed by 1 g orally every 6 hours. Patients should be encouraged to take fluids and one teaspoonful of sodium bicarbonate twice daily.

    Seronegative women who acquire toxoplasmosis during pregnancy may be treated with spiramycin 1 g orally every 8 hours. The drug can be obtained on a compassionate basis from the U.S. Food and Drug Administration (FDA) by calling 301-827-2335.

    Infants with congenital toxoplasmic retinochoroiditis may be treated with pyrimethamine given at a dosage level of 1 mg/kg/day orally to a maximal dose of 25 mg per day. The dose should be reduced to 0.5 mg/kg/day after 4 days of treatment. Newborns can be treated with pyrimethamine once every 3 days. This is because the half-life of pyrimethamine is 2 to 3 days. In view of the adverse effects of pyrimethamine on the hematopoietic system, folinic acid should be given at a dosage level of 3 mg orally every other day, and white blood cell and platelet counts should be closely monitored. Sulfadiazine may be given in conjunction with pyrimethamine at a dosage of 100-150 mg/kg/d orally in 4 divided doses for 4 weeks.

    Other antimicrobial agents that have been used for the treatment of ocular toxoplasmosis include azithromycin, clindamycin, minocycline, and atovaquone.

    Azithromycin has been shown to be effective alone or in combination in the treatment of murine toxoplasmosis.5 Azithromycin may be given in combination with sulfamethoxazole/trimethoprim (800/160 mg (Bactrimâ DS).2

    Prevention of Ocular Tissue Damage

    Inflammatory cells and their cytokines may lead to structural damage of the retina and choroid. Corticosteroids are usually added to the therapeutic regimen when vision-threatening lesions are observed. Vision-threatening lesions include the macula, paramacular areas, maculopapillary bundle, the optic nerve head, and extensive vitreous reaction. Oral corticosteroids should not be given without antimicrobial coverage. In paramacular and macular toxoplasmosis, periocular injection of corticosteroids may be used with caution. Posterior subtenon injection of triamcinolone acetonide 40 mg may be given.

    The use of posterior subtenon's injection of corticosteroids carry significant risk of local suppression of the immunity and exacerbation of the disease. The use of periocular steroids in ocular toxoplasmosis remains controversial.

    Intravitreal injection of triamcinolone acetonide has been reported as an adjunct in the treatment of severe ocular toxoplasmosis.6 The safety of intravitreal triamcinolone remains to be determined. Intravitreal injection of dexamethasone and clindamycin has been used in a limited number of cases.

    Prevention of Recurrences

    Prevention of recurrences of toxoplasmic retinochoroiditis may prevent loss of vision. Patients with paramacular toxoplasmosis may be given antimicrobial prophylaxis to prevent recurrences. Long-term intermittent trimethoprim/sulfamethoxazole prophylactic treatment can prevent or decrease the recurrences of toxoplasmic retinochoroiditis.7 The treatment consists of the administration of sulfamethoxazole/trimethoprim 800/160 mg 1 tablet every 3 days.

    Recurrences of toxoplasmic retinochoroiditis may occur following LASIK and phacoemulsification with posterior chamber intraocular lens implantation.8,9 It is therefore recommended that prophylactic treatment be given to patients 2 days prior to surgery and to be continued for a period of 1 week.

    Vision Rehabilitation

    Patients with ocular toxoplasmosis who develop vitreous exudates and vitreous membranes causing decrease in vision or retinal traction may be helped by vitrectomy. Vitrectomy should not be performed during periods of active inflammation within the eye.

    Toxoplasma cysts may occur in areas funduscopically normal retina. The site of toxoplasma cysts may not be determined by ophthalmoscopy. Photocoagulation or cryotherapy, therefore, may not eradicate the toxoplasma cysts from the retina.

    Choroidal neovascularization may occur in patients with toxoplasmic retinochoroiditis. Verteporfin photodynamic therapy has been shown to be safe and effective in the treatment of subfoveal choroidal neovascularization associated with toxoplasmosis.10

    The safety and efficacy of antiangiogenesis agents such as bevacizumab and ranibizumab in the treatment of choroidal neovascular membrane and cystoid macular edema in ocular toxoplasmosis remain to be elucidated.

    References

    1. Tabbara KF. Ocular Toxoplasmosis. In: Tasman W, Jaeger EA, eds. Uvea Section, Duane's Clinical Ophthalmology. Baltimore, MD; Lippincott Williams & Wilkins; 2008.
    2. Bosch-Driessen LH, Verbraak FD, Suttorp-Schulten MS, van Ruyven RL, Klok AM, Hoyng CB, Rothova A. A prospective, randomized trial of pyrimethamine and azithromycin vs pyrimethamine and sulfadiazine for the treatment of ocular toxoplasmosis. Am J Ophthalmol. 2002;134(1):34-40.
    3. Soheilan M, Sadoughi MM, Ghajarnia M, Dehghan MH, Yazdani S, Behboudi H, Anisian A, Peyman GA. Prospective randomized trial of trimethoprim/sulfamethoxazole versus pyrimethamine and sulfadiazine in the treatment of ocular toxoplasmosis. Ophthalmology. 2005;112(11):876-882.
    4. Holland GN, Lewis KG. An update on current practices in the management of ocular toxoplasmosis. Am J Ophthalmol. 2002;134(1):102-114. Erratum in: Am J Ophthalmol. 2002;134(6):944.
    5. Tabbara KF, Hammouda E, Tawfik A, Al-Omar OM, Abu El-Asrar AM. Azithromycin prophylaxis and treatment of murine toxoplasmosis. Saudi Med J. 2005;26(3):393-397.  
    6. Backhouse O, Bhan KJ, Bishop F. Intravitreal triamcinolone acetonide as an adjunct in the treatment of severe ocular toxoplasmosis. Eye. 2008;Feb 8 [Epub ahead of print]
    7. Silveira C, Belfort R Jr, Muccioli C, Holland GN, Victora ACG, Horta BL, Yu F, Nussenblatt RB. The effect of long-term intermittent trimethoprim/sulfamethoxazole treatment on recurrences of toxoplasmic retinochoroiditis. Am J Ophthalmol. 2002;134(1):41-46.
    8. Bosch-Driessen LH, Plaisier MB, Stilma JS, Van der Lelij A, Rothova A. Reactivations of ocular toxoplasmosis after cataract extraction. Ophthalmology. 2002;109(1):41-45.
    9. Barbara A, Shehadeh-Masha'our R, Sartani G, Garzozi HJ. Reactivation of ocular toxoplasmosis after LASIK. J Refract Surg. 2005;21(6):759-761.
    10. Mauget-Faÿsse M, Mimoun G, Ruiz-Moreno JM, Quaranta-El Maftouhi M, De Laey JJ. Postelmans L, Soubrane G, Defauchy M, Leys A. Verteporfin photodynamic therapy for choroidal neovascularization associated with toxoplasmic retinochoroiditis. Retina. 2006;26(4):396-403.

    Author Disclosure

    Dr. Tabbara states that he has no financial relationship with the manufacturer or provider of any product or service discussed in this article or with the manufacturer or provider of any competing product or service.