A 30 year old male presented with unilateral blurred vision, pain, photophobia, and redness in the right eye for one week. On examination, his visual acuity in the right eye was 20/200 “E” at 1 foot and 20/20 in the left eye. The intraocular pressures were 27mmHg and 21mmHg in the right and left eyes, respectively. He had a small afferent pupillary defect in the right eye.

The slit lamp examination of the right eye revealed a mildly inflamed conjunctiva with moderate anterior chamber cell and dense vitreous cell. There was optic disc edema and a large white retinal lesion in the macula with adjacent hyperpigmentary changes. There was perivenular sheathing throughout the posterior pole. The exam of the left eye was unremarkable. A review of social history revealed that the patient had grown up around cats. He denied any autoimmune disease or known infectious disorders.

The patient was started on sulfamethoxazole-trimethoprim 800-160mg (Bactrim® DS) twice daily and clindamycin 300mg three times daily. The patient was also advised to use cyclopentolate. Oral corticosteroids were discussed given the macular involvement, and safety infectious labs including Quantiferon gold, FTA, and RPR were ordered. Additionally, serum toxoplasmosis IgG/IgM was drawn and returned with a significantly elevated IgG titer.

At a 1 week follow up, the vision in the right eye was relatively stable at counting fingers at 3 feet. The patient was started on 30mg prednisone, prednisolone acetate 1% drops four times daily, and continued on the same oral antibiotics. After 3 weeks of treatment, the vision had improved to 20/400, and the inflammatory reaction had improved dramatically. The macular lesion was less inflamed and had atrophy forming at the edges of the lesion. The patient was asked to stop the clindamycin, continue the Bactrim®, and begin a slow taper of the oral prednisone, down 5mg weekly. Once the steroid was discontinued, Bactrim® was reduced to three times weekly as a prophylactic dose for one year.

Toxoplasmosis gondii

Toxoplasmosis gondii is a protozoan parasite that is surprisingly common amongst the world’s population. One study from 2011-2014 estimated that the seroprevalence of T. gondii in the United States was 11%[1]. The incidence is considerably higher in other areas of the world like Central and South American countries, where it is estimated to be between 30-90%[2]. It can be transmitted in one of three ways: foodborne via undercooked meat, animal-to-human via contact with animal – typically cat – feces, or mother-to-child if a primary infection occurs during pregnancy. In foodborne and animal-to-human transmission, the infectious protozoa spreads via immature eggs called oocytes. Once the oocytes are ingested, the parasite establishes presence inside the new host. Inside a host, the parasite can pass into the blood stream and through vascular barriers, forming local cysts throughout the body in various tissues, including the retina, usually in an inactive state[3]. In most cases, humans who are infected with T. gondii are asymptomatic or have a mild, self-limiting initial infectious phase. Occasionally, particularly in patients who are immunocompromised, infections or reactivations can pose significant risk to life or bodily function. 

Toxoplasmosis in the eye – straightforward diagnosis and treatment?

Although T. gondii is the most common cause of infectious posterior uveitis worldwide and is known to have a classic “headlight in the fog” appearance owing to the white retinochoroidal inflammatory lesion visible through vitritis, it can still be difficult to diagnose with certainty. Numerous case reports have shown that toxoplasmosis, particularly in immunocompromised individuals, can take on a severe form and masquerade other conditions such as acute retinal necrosis [4]. A careful exam, thorough patient history, and often even blood serum and/or aqueous laboratory testing are necessary to confirm suspicions. 

Typical clinical findings of active toxoplasmosis include anterior chamber cell, vitritis, and the presence of inflammatory retinochoroidal lesion(s) with overlying haze and adjacent hyperpigmented scars. The scars and active lesion are often generally located in the posterior pole. Other possible findings include intra-arterial white Kyrieleis plaques, retinal hemorrhaging, elevated intraocular pressure, periphlebitis, and neuroretinitis[3, 5].

Treatment strategies for an active case of ocular toxoplasmosis vary. There are a few reasons for this. The reactivation and local inflammatory response from ruptured intraretinal cysts is generally self-limiting. In an immune competent patient, a case of retinochoroiditis typically lasts about one to two months. Because of this, if the active lesion is small and peripheral, some physicians may elect to observe without treatment. A patient with an active lesion in the posterior pole has a higher likelihood of vision-threatening complications such as macular edema, optic nerve edema, and macular scarring, and therefore treatment is typically indicated. Oral treatment for ocular toxoplasmosis includes antibiotics such as clindamycin, sulfadiazine, sulfamethoxazole-trimethoprim; the antiparasitic pyrimethamine; and corticosteroids like prednisone. Topical ophthalmic medications like corticosteroids, cycloplegics, and aqueous suppressants may also be indicated depending on the clinical findings. Treatment duration is long, generally lasting anywhere from 4-6 weeks for active disease.

When treatment is indicated, there are multiple strategies and combinations used by specialists. It is important to note that there is not one single widely accepted treatment protocol. The so-called “classic” treatment strategy involves a combination of pyrimethamine, sulfadiazine and a systemic corticosteroid (typically prednisone). Folinic acid should be prescribed alongside pyrimethamine to reduce the chance of bone marrow suppression, and regular labs should be drawn. Another  treatment strategy includes a combination of sulfamethoxazole-trimethoprim and oral prednisone with or without clindamycin. One study comparing medical treatment vs observation alone showed that although initiating treatment did not shorten the duration of disease nor decrease the risk of reactivation, it did reduce the size of the retinochoroidal lesion(s)[6]. This led to the commonly held belief that paramacular lesions should be treated. Lastly, some physicians recommend prophylactic dosing of Bactrim®, as intermittent dosing (every 2-3 days) has been shown to significantly reduce the risk of recurrence [7, 8]. Therefore, it should be considered in cases of macular lesions.

In summary, T. gondii is an exceedingly common pathogen worldwide, and it may cause significant ocular morbidity in certain individuals. Although diagnostic and treatment strategies may vary widely based on patient characteristics and physician preferences, it is important to be aware of the options available to these patients and advocate for their expeditious and thorough care.  

Figure 1: Right fundus on presentation with large macular inflammatory lesion and adjacent chorioretinal scars near the optic nerve.


Figure 2: Right macula OCT on presentation reveals significant retinal thickening and hyperreflectivity with intraretinal spaces and pinpoint vitreous opacities consistent with inflammatory cells.

Figure 3: 2 month follow up shows clear media with a macular scar and pigmentary changes.


Figure 4: 2 month follow up. OCT reveals significant atrophy and disorganization of retinal layers at the macula.


  1. Jones, J.L., et al., Toxoplasma gondii Infection in the United States, 2011-2014. Am J Trop Med Hyg, 2018. 98(2): p. 551-557.
  2. Aguirre, A.A., et al., The One Health Approach to Toxoplasmosis: Epidemiology, Control, and Prevention Strategies. Ecohealth, 2019. 16(2): p. 378-390.
  3. Kalogeropoulos, D., et al., Ocular toxoplasmosis: a review of the current diagnostic and therapeutic approaches. Int Ophthalmol, 2022. 42(1): p. 295-321.
  4. Moshfeghi, D.M., et al., Diagnostic approaches to severe, atypical toxoplasmosis mimicking acute retinal necrosis. Ophthalmology, 2004. 111(4): p. 716-25.
  5. Westfall, A.C., et al., Toxoplasmosis retinochoroiditis and elevated intraocular pressure: a retrospective study. J Glaucoma, 2005. 14(1): p. 3-10.
  6. Rothova, A., et al., Therapy for ocular toxoplasmosis. Am J Ophthalmol, 1993. 115(4): p. 517-23.
  7. Silveira, C., et al., The effect of long-term intermittent trimethoprim/sulfamethoxazole treatment on recurrences of toxoplasmic retinochoroiditis. Am J Ophthalmol, 2002. 134(1): p. 41-6.
  8. Fernandes Felix, J.P., et al., Trimethoprim-Sulfamethoxazole Versus Placebo in Reducing the Risk of Toxoplasmic Retinochoroiditis Recurrences: A Three-Year Follow-up. Am J Ophthalmol, 2016. 170: p. 176-182.