InternationalOphthalmology14: 349-351, 1990. 9 1990KluwerAcademicPublishers.Printedin theNetherlands.

Ocular toxoplasmosis Khalid F. Tabbara

Department of Ophthalmology, College of Medicine, King Saud University, Riyadh, Kingdom of Saudi Arabia; Supported in part by the Saudi Eye Foundation, Jeddah, Saudi Arabia Accepted 12 April 1990

Abstract

Toxoplasmosis is a common infection of man and animals. The disease is widespread in nature and has a worldwide distribution. The infection is caused by the organism Toxoplasma gondii which was first isolated by Nicolle and Manceaux in Tunis from a North African rodent. The disease can be congenital or acquired with a variety of clinical manifestations that may range from a subclinical course to a generalized infection with fatal outcome. The ocular manifestations of the disease include sudden onset of floaters with blurring of vision. Toxoplasmosis causes a localized necrotizing retinitis with inflammation of the subjacent choroid. The retina sustains the primary injury and the major damage.

Toxoplasmosis is a zoonotic disorder affecting both man and animals [1]. The disease is widespread in nature and is considered to be the most common cause of infection of the retina [2].

Toxoplasma gondii Toxoplasmosis is caused by an obligate intracellular parasite known as Toxoplasmagondii. The term toxo is derived from the Greek word toxon or arc because of the crescentic shape of the parasite, and gondii because it was first recovered from a North African rodent in Tunis known as Ctenodactylus gundi. Under light microscopy Toxoplasma organisms can be observed to perform interesting undulating movement having a conoid at its rostral end with an ability to thrust forward, protrude and retract. These actions are mediated by a fibrillary cytoskeletal structure and can be blocked by cytochalasin D which is known to interfere with the synthesis of actin. Toxoplasma has no flagella. Since this protozoon is an obligate intracellular

parasite and cannot survive or multiply in the extracellular space, the initial entry into the host cell is a critical step in the pathogenesis of the disease. Toxoplasma tachyzoites thrust their conoid outward at the time of invasion into the cell. Entry into retinal cells is by active invasion [3-4]. At the time of contact of the Toxoplasma with the cell membrane the differentiated organelles known as 'rhoptries' secrete enzymes which lead to disruption of the plasmalemma of the host cell and allows the organism to get access into the cytoplasm. The process of active penetration under laboratory conditions takes 30 seconds [4].

Transmission of the disease

Man can acquire toxoplasmosis by the inhalation of the sporozoite in oocyst or ingestion of the oocysts, by the ingestion of toxoplasma cysts containing bradyzoites in undercooked meat, and by transplacental organ transplantation or accidental transmission of the tachyzoite [1, 5, 6].

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Ocular manifestations The disease may be congenital or acquired with clinical manifestations ranging from asymptomatic subclinical course to a generalized fulminant infection with fatal outcome. The ocular manifestations consist of a localized area of necrotizing retinitis. The subjacent choroid may also eventually become affected by the inflammatory cells. The retina sustains the primary insult and the major damage. The ocular lesions consist of a soft fluffy white infiltrate surrounded by retinal edema. The ocular lesion may be single or multiple, small or large reaching several disc diameters in size and sometimes seen as an elevated lesion surrounded by a pale orange background [11. Since the organism is an obligate intracellular parasite, it has no interest in leaving the retinal tissues and invading the vitreous cavity which is an acellular structure. Invasion of the vitreous by inflammatory cells in cases of toxoplasmic retinitis is a hypersensitivity phenomenon secondary to spillage or to diffusion of the toxoplasma antigen into the vitreous. Retinal arteritis and phlebitis may be associated with toxoplasma retinochoroiditis. This may lead to vascular occlusion. Subretinal neovascular membranes may be seen in the aftermath of the inflammatory process. Cystoid macular edema is commonly seen in patients with ocular toxoplasmosis and may lead to irreversible damage to the photoreceptors. Healing of the retinochoroiditis lesion is associated within vitreous reaction and retinal pigment epithelial cell proliferation and scar formation.

Complications Retinal complications include the formation of retinal holes, scars, retinal vascular occlusions secondary to retinal vasculitis and cystoid macular edema. Optic atrophy may be seen in some patients. The association of ocular toxoplasmosis and Fuchs' Hetrochromic iridocyclitis has been previously observed [7]. Subretinal vascularization may also be seen. The retinochoroiditic scars are not

sterile and may harbor the encysted form of the parasite. Rupture of these cysts for one reason or another leads to the recurrence of toxoplasmic retinochoroiditis. Recurrence of ocular toxoplasmosis may result from systemic or local immunologic suppression. This suggests the persistence of toxoplasma cysts in the retinochoroiditic scars and when the patient's immune mechanisms are suppressed a recurrence of the disease occur. The recurrence, therefore, is not a hypersensitivity phenomena to toxoplasma antigens but secondary to active proliferation of the parasite in the retinal tissues.

Experimental toxoplasmosis When we injected toxoplasma organisms into the peritoneal cavities of eleven Swiss-Webster mice, we were able to find Toxoplasmacysts in the retina of nine of the infected mice. These cysts are seen surrounded by inflammatory mononuclear cells and plasma cells which have the unique function of producing antibodies against toxoplasma. This suggested to us that the cyst wall engineered and built by the parasite represents a defensive phase of the organisms to withstand the hostile environment and to evade the revages of the immune system. This was corroborated in the laboratory. Toxoplasma organisms when inoculated onto tissue culture cell line destroys the cells within one week after inoculation. When anti toxoplasma antibody with complement is added to the tissue culture medium, the organisms stop its cell destruction and form cysts [8]. It is a generally believed that toxoplasmic retinochoroiditis is a recrudescence of congenital toxoplasmosis. Over the past decade we have seen several cases of ocular toxoplasmosis associated with or followed an episode of acquired toxoplasmosis. There is evidence to believe, therefore, that toxop!asmic retinochoroiditis may occur with systemic toxoplasmosis [9]. The prevalence of retinochoroiditis in patients with acquired systemic toxoplasmosis is difficult to determine because of the frequent asymptomatic nature of the disease. In experimental animals we have found that antitoxoplasma antibodies and toxoplasma antigens

351 may be detected in the vitreous specimens of rabbits with toxoplasmic retinochoroiditis [10]. The antigen is detected at the height of activity of the disease and antibodies are found in the vitreous of all infected eyes at six weeks after the onset of the disease.

Laboratory diagnosis Laboratory tests include the Toxoplasma dye test of Sabin and Feldman which may be positive at a very low titer and the indirect fluorescent antibody test which can detect IgG and IgM antibodies to Toxoplasma gondii. Other tests for toxoplasmosis are the hemaglutination and E L I S A . X-ray of the skull helps in cases of suspected congenital toxoplasmosis.

Treatment Treatment of ocular toxoplasmosis consists of pyrimethamine and sulfadiazine with folinic acid. Other therapeutic modalities include the use of spiramycin, clindamycin, or minocycline with or without sulfadiazine. Corticosteroids are used in cases of vision threatening lesions. In conclusion, toxoplasmosis is a c o m m o n infection of the retina and should always be considered in the differential diagnosis of unilateral posterior uveitis and panuveitis.

References 1. Tabbara KF. Toxoplasmosis. In: Duane TD, ed. Clinical Ophthalmology. Philadelphia, Harper and Row, 1987; 4(46): 1-23. 2. Tabbara KF. Management of ocular toxoplasmosis. Trans Pac Coast Oto-ophthalmol Soc 1982; 63: 23. 3. Nichols B, Chiappino ML. Cytoskeleton of Toxoplasma gondii. J Protozool 1987; 34(2): 217-26. 4. Nichols BA, O'Connor GR. Penetration of mouse peritoneal macrophages by the protozoon Toxoplasma gondii: New evidence for active invasion and phagocytosis. Lab Invest 1981;44: 324. 5. Teutsch SM, Juranek DD, Sulzer A, et al. Epidemic toxoplasmosis associated with infected cats. N Engl J Med 1979; 300: 695. 6. Desmonts G, Couvreur J. Toxoplasmosisin pregnancyand its transmission to the fetus. Bull Ny Acad Med 1974; 50: 146. 7. De Abreu MT, Belfort R Jr, Hirata PS. Fuchs' heterochomiccyclitisand ocular toxoplasmosis. Am J Ophthalmol 1982; 93: 739. 8. Shimada K, O'Connor GR, Yoneda C. Cyst formation by Toxoplasma gondii (RH strain) in vitro. Arch Ophthalmol 1974; 92: 496. 9. Michelson JB, Shields JA, McDonald R, et al. Retinitis secondary to acquired systemic toxoplasmosis with isolation of the parasite. Am J Opthalmol 1978; 86: 548. 10. RollinsDF, Tabbara KF, O'Connor GR, et al. Detection of toxoplasma antigen and antibodyin ocular fluids in experimental ocular toxoplasmosis. Arch Ophthalmol 1983; 101: 455.

Address for offprints: K. Tabbara, P.O. Box 55307, Riyadh 11534Saudi Arabia

Ocular toxoplasmosis.

Toxoplasmosis is a common infection of man and animals. The disease is widespread in nature and has a worldwide distribution. The infection is caused ...
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