Color fundus photograph shows toxoplasmic scar in a patient with congenital toxoplasmosis
Clinical Features
Wide field fundus photograph shows yellow-white retinal focus with severe vitritis (headlight in the fog)
SD-OCT image demonstrates disorganized neurosensory retinal layers and choroidal thickening beneath the active lesion
Color fundus photograph shows multiple toxoplasmic retinochoroidal scars
Color fundus photograph shows macular toxoplasmic retinochoroidal scar
Color fundus photographs show recurrent toxoplasmosis lesions. (a) Active lesions adjacent to the old lesion. (b) After 3 months of treatment, the borders of active lesions become more defined. (c) Two month later, the lesion recurred at the border of healed scar. (d) The lesion healed after 2 months of treatment
Ocular toxoplasmosis can result in permanent visual loss because of retinal necrosis, uveitis, and its complications. The complications of ocular toxoplasmosis include chronic iridocyclitis, cataract formation, secondary glaucoma, band keratopathy, cystoid macular edema, retinal neovascularization, epiretinal membrane, retinal detachment, and optic atrophy secondary to optic nerve involvement (London et al. 2011).
Laboratory Techniques
Although the diagnosis of ocular toxoplasmosis is usually based on typical clinical presentation, laboratory tests can be helpful when the clinical diagnosis cannot be made definitely by a funduscopic examination. Serologic tests are used to confirm past exposure to T. gondii. The IgM and IgG antibodies to T. gondii appear in the serum within 1–2 weeks after infection (Marcolino et al. 2000). IgM levels increase within the first week and become undetectable after 6–9 months. IgG levels can often persist for years after the acute infection, and there is a high prevalence of such antibodies in the general population giving false-positive results (Ongkosuwito et al. 1999). Therefore, elevated levels of antibodies alone should not be considered as an evidence of recent infection, nor should low serum IgG levels be considered as inactive disease.
The advance in molecular biology techniques has enabled the identification of T. gondii DNA in the aqueous humor and the vitreous by polymerase chain reaction (PCR) (Fekkar et al. 2008). It has even allowed the identification of T. gondii DNA in ocular tissue sections of patients with presumed ocular toxoplasmosis when organisms could not be identified on histopathologic examination. However, the sensitivity of PCR in patients meeting clinical diagnostic criteria for ocular toxoplasmosis is variable, and the sensitivity of PCR also depends on the immune status of the patient (Garweg et al. 2011).
Management
In immunocompetent patients, toxoplasmic retinochoroiditis is usually a self-limited infection and generally resolves spontaneously over a period of 1–2 months (Butler et al. 2013). Considering this benign natural history and the potential toxicity of anti-parasitic medication, the risk of treatment may be greater than any benefit provided. However, treatment is recommended for immunocompetent patients with active inflammation who have reduced visual acuity, lesion located within the vascular arcades or adjacent to the optic disc, lesion larger than two optic disc diameters to reduce the chance of vision loss, and/or vitreous haze above grade 1+ (Holland and Lewis 2002). There is no cure for toxoplasmosis infection since the tissue cysts are resistant to the available drugs and remain viable for many years (Stanford et al. 2003). Therefore, the aim of the treatment of ocular toxoplasmosis is to arrest parasite multiplication during the active stage and to minimize damage to the retina and optic disc (Holland and Lewis 2002; de-la-Torre et al. 2011). Atypical presentations and disease in immunocompromised patients require immediate treatment (Smith and Cunningham 2002).
Medical Therapy
The combination of pyrimethamine (25–50 mg daily orally in one to two doses) (Holland and Lewis 2002) and sulfadiazine (1 g four times daily orally) (Holland and Lewis 2002), which have a synergistic effect on different steps of the nucleic acid synthesis in T. gondii, and corticosteroids (often in the form of prednisone) have remained as the “classic therapy” or “triple-drug therapy” (Eyles and Coleman 1953). Patients treated with classic therapy showed a greater reduction in the size of the retinal lesion than patients receiving other treatments or no treatment (Rothova et al. 1993). However, this classical treatment may have some risks that depend on patient susceptibility to drug toxicity or allergic reactions.
An alternative to classic treatment, trimethoprim-sulfamethoxazole (160–800 mg twice daily orally) (Holland and Lewis 2002) is an attractive option for reasons that include low cost, less adverse effects, and good compliance due to the reduced number of daily pills. This drug combination of trimethoprim-sulfamethoxazole plus corticosteroids was shown to have similar efficacy to classic treatment in a randomized clinical trial (Holland 2005; Soheilian et al. 2005). However, sulfonamide-related reactions may still occur (Soheilian et al. 2005).
Other drugs, such as clindamycin (300 mg four times daily orally) (Holland and Lewis 2002), have also been used. It is often added to triple therapy, which is then referred to as “quadruple therapy.” In other situation, clindamycin has been substituted for pyrimethamine.
The duration of treatment depends on the individual and patients’ clinical situations. It is recommended that corticosteroids should not be used without anti-toxoplasmic drugs in order to avoid the worsening of the infection (Stanford and Gilbert 2009).
Intravitreal Injection
Intravitreal injection of clindamycin and dexamethasone as local treatment for ocular toxoplasmosis is a promising approach (Lasave et al. 2010; Soheilian et al. 2011). Because intravitreal drug administration bypasses ocular barriers, high concentration of drug can be delivered directly to the intraocular tissues, thus reducing systemic side effects. Intravitreal clindamycin (1 mg) and dexamethasone (400 μg) were shown to have similar efficacy in terms of reduction in lesion size, increase in visual acuity, and decrease in vitreous inflammation to triple therapy in a randomized clinical trial (Soheilian et al. 2011).
Local treatment appears particularly useful for patients with recurrent infection and for those systemic side effects of the drug are a concern, such as pregnant women. On the other hand, the local treatment would not be recommended in immunocompromised patients (Butler et al. 2013).
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