Handbook of Ocular Disease Management

TOXOPLASMOSIS

Active Toxoplasmosis

Inactive Toxoplasmosis Scar

SIGNS AND SYMPTOMS
The symptoms associated with ocular toxoplasmosis include unilateral, mild ocular pain, blurred vision and new onset of floating spots. Patients often describe their vision as hazy. Clinical findings may include granulomatous iritis, vitritis, optic disc swelling, neuroretinitis, vasculitis and retinal vein occlusion in the vicinity of the inflammation, in the actively involved eye. Funduscopically, active toxoplasmosis presents with white-yellow, choreoretinal lesions and vitreous cells. There may be old, inactive lesions in the fellow eye. Toxoplasmosis can produce cystoid macular edema and choroidal neovascularization.

PATHOPHYSIOLOGY
Toxoplasmosis is a disease provoked by the obligate intracellular protozoan Toxoplasma gondii. It is found in a variety of mammal and bird hosts. The most common intermediate host is the cat. It is one of the most frequent causes of retinochoroiditis in humans, with more than 60 percent of the United States population and up to 75 percent of the world's general population possessing some seropositive findings.

The systemic symptoms found in congenital toxoplasmosis consist of convulsions, calcification of the arterioles and choreoretinitis. In adults, toxoplasmosis is often contracted without sickness. A small percentage of individuals encounter self-limiting, flu-like symptoms at the time of inoculation.

Toxoplasma exists in humans in two forms: (1) actively motile tachyzoites and (2) encysted Toxoplasma gondii called brachyzoites. The oocysts that contain the organisms which produce infection are excreted in fecal material and may lie dormant in the soil until ingested by other animals, resulting in infection.

Human infection may occur from ingestion of contaminated or undercooked meat and dairy products, direct or indirect ingestion of cat feces and transplacental transmission from an infected mother to the fetus. Toxoplasmosis can only be transmitted to a fetus during maternal parastemia. Congenital toxoplasmosis accounts for the majority of cases encountered in clinical practice.

In most cases, the body is primed for infection or toxoplasmosis reactivation by an immune system failure. This may occur following contraction of human immunodeficiency syndrome (HIV) or with medical immunosupression following organ transplantation.

The inflammatory fundus lesions are composed of mononuclear cells, with a liberation of lymphocytes, macrophages, epithelioid and plasma cells. The resulting retinal vasculitis contributes to the breakdown of the blood-retinal barrier and leads to a compromise in retinal function, with subsequent destruction and thickening.

MANAGEMENT
The goal of management is twofold: (1) eradicate the parasite and (2) suppress the inflammatory response. The classic treatment regimen combines pyrimethamine (a 75mg loading dose, followed by 25mg PO BID administration) with sulfadiazine (2g loading dose, then 1g PO QID for 4 to 6 weeks). Both medications inhibit the folic acid metabolism necessary for toxoplasmosis to survive. Concurrent folinic acid, 3 to 5mg PO twice weekly helps to minimize any bone marrow toxicity produced by the pyramethamine.

Alternative antibiotic treatments include: (1) clindamycin, 300mg, PO QID used with sulfadiazine, for four to six weeks, (2) tetracycline, 2g loading then 250mg PO QID and sulfadiazine for four to six weeks, or (3) trimethoprim/sulfamethoxazole 160/800mg, one tablet PO BID, with or without clindamycin or prednisone, for the same duration.

In otherwise normal individuals, after beginning antibiotic therapy, add oral steroids at a dose of 20 to 80mg PO daily for four to six weeks. Periocular steroids are never indicated. Oral steroids without systemic antibiotics are expressly contraindicated.

Manage the anterior ocular inflammation with a cycloplegic that is appropriate for the disease's severity and a topical steroid Q2H/QID.

Systemic laboratory testing is indicated in active cases. The Sabin-Feldman methylene blue dye test (for Toxoplasma gondii), Serum antitoxoplasma antibody titer (for Toxoplasma gondii), Fluorescent Treponemal Antibody absorption test (for syphilis), purified protein derivative (for tuberculosis), chest x-ray (for sarcoid and TB), Toxocara Enzyme Linked Immunofluorescent Assay (for Toxocara canis) and Human Immunodefeciency Virus titer (for HIV) are among the important tests to order.

CLINICAL PEARLS

Since the organism may remain viable for up to 25 years and reactivation attacks are common, patient education is vital. If an outbreak is discovered in a community, provide education regarding the consumption of uncooked or under-cooked foods and the danger of untidy cats and/or their litter boxes.
In patients who have active infection, consider HIV/AIDS, especially if no other obvious means of immunosuppression are present. Surgical modalities, such as laser photocoagulation and cryopexy, have less value and are traditionally only recommended when the other modalities have failed.

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