A 25 year old male was referred to Illinois Retina Associates for blurred vision in the right eye for the past week. There were also floaters but not flashing lights or pain. No problems were noted in the left eye. He had no known systemic illnesses. He is on no systemic or ocular medications. He has a history of trauma to the left eye and subsequently underwent cataract surgery in that eye without subsequent issue.
Vision on presentation was 20/150 in the right eye and 20/20 in the left. Pressures were normal at 13 mmHg and 16 mmHg in the right and left eyes, respectively. The anterior segment exam was unremarkable. Posterior segment exam showed 2+ vitreous cell and a superonasal chorioretinal scar with adjacent whitening in the right eye as shown below (Figure 1) and pigmented ‘quiet’ scar noted directly nasally (Figure 2).
- Autoimmune disease
Fluorescein Angiography showed no leakage either eye with some staining of the white fibrotic area in the right eye.
Systemic workup included toxoplasmosis IgG and IgM, Quantiferon Gold, rapid plasma reagin, complete blood count, erythrocyte sedimentation rate and chest X-ray. This was normal or negative with the exception of toxoplasmosis IgG.
The patient was initiated on therapy including triple therapy for toxoplasmosis with sulfasalazine, pyrimethamine and leucovorin and treatment of inflammation with oral and topical steroids. The patient’s vision improved slowly with therapy back to 20/25 as the vitreous debris slowly cleared.
The vision slowly began to improve as the vitreous debris cleared in response to treatment. Four months after presentation he was back to 20/25 with only minimal vitreous debris remaining. The whitening of the retina had regressed and he remained quiet as he was weaned off of steroid treatment and the antibiotics were stopped. Unfortunately, a month after cessation of therapy the disease reactivated at the posterior edge of the lesion (Figure 3). All medications were restarted.
Toxoplasmosis is a disease caused by the intracellular parasite Toxoplasma gondii. It is thought to be the most common cause of posterior uveitis worldwide. Most people are exposed to toxoplasmosis in their lifetime, only a minority of these will develop ocular disease. Many who do develop ocular disease can be safely watched, as long as the lesion is not near the macula.
For those with vision threatening disease or those who are immunocompromised, therapy with multiple antibiotics and steroid is recommended. The conventional combination is systemic pyrimethamine, sulfadiazine, and corticosteroids. Oral clindamycin may be considered as an additional agent. There has also been evidence to support use of intravitreal clindamycin and dexamethasone as an alternative to oral treatment.
Arantes, T. E. F., Silveira, C., Holland, G. N., Muccioli, C., Yu, F., Jones, J. L., . . . Belfort Jr., R. (2015). Ocular involvement following postnatally acquired toxoplasma gondii infection in Southern brazil: A 28-year experience. American Journal of Ophthalmology, 159(6), 1002-1012.e2. doi:http://dx.doi.org.ezproxy.rush.edu/10.1016/j.ajo.2015.02.015
Grigg, M. E., Dubey, J. P., & Nussenblatt, R. B. (0727). Ocular toxoplasmosis: Lessons from brazil
Soheilian, M., Ramezani, A., Azimzadeh, A., Sadoughi, M. M., Dehghan, M. H., Shahghadami, R., . . . Peyman, G. A. (2011). Randomized trial of intravitreal clindamycin and dexamethasone versus pyrimethamine, sulfadiazine, and prednisolone in treatment of ocular toxoplasmosis. Ophthalmology, 118(1), 134-141. doi:http://dx.doi.org.ezproxy.rush.edu/10.1016/j.ophtha.2010.04.020