Optometry Dx: Cat’s Got Your Eye


  • Figure 1. The fundus image shows a 27-year-old patient with toxoplasmosis chorioretinitis who was experiencing blurred vision.

  • Figure 2. The patient also had elevated intraocular pressure in her left eye (32 mm Hg). She was managed with Timoptic 0.5% and seen for a follow-up visit 2 days later, when this image was taken.

  • You can skip this ad in 3 seconds.
  • Figure 3. A year after her initial presentation, a densely pigmented toxoplasmosis scar was evident.

A 27-year-old woman — a graduate student from Brazil — suddenly noticed some spots in her left eye and, 2 days later, the vision in her left eye became blurred and she was seen by our eye service. There was a finding, a small inflammatory lesion in the superotemporal fundus of her left eye (Figure 1). Otherwise the rest of the retina appeared normal, as was the right eye. Her vision was correctable to 20/20 OD, 20/25 OS. Pupils and finger counting fields were normal. Her intraocular pressures were 14 mm Hg OD and 32 mm Hg OS. She had no notable systemic history and did not use any medications. A slit lamp examination revealed occasional cells in the anterior chamber and 2+ cells in the posterior chamber of the left eye. Gonioscopy demonstrated both angles open to ciliary body band. She was put on Timoptic 0.5% to be applied to her left eye twice daily to reduce her IOP, and she was seen 2 days later (Figure 2). 

At the 2-day follow-up, the chorioretinal lesion had become more active, and she reported that her vision was “like looking through plastic.” More cells were noted in the vitreous, but the lesion was still limited to the superotemporal area, and the macular area and optic nerve were uninvolved. The patient was immediately referred to a retinal specialist. 

The patient was diagnosed with toxoplasmosis chorioretinitis. Toxoplasmosis is a protozoan that is often acquired in utero, and it can predispose to recurrences adjacent to the chorioretinal scars.1,2 Primary toxoplasmosis is not contagious directly from another person, but by ingestion of contaminated food and water, handling raw meat, or cat feces. The patient was told that the protozoan organisms that cause the cysts can not be killed by current drug treatments, and remain viable for many years. Current drug combinations can only attempt to prevent the recurrence of the organism. The patient was informed of the possibility of recurrences, and told to contact her eye specialist immediately if she experienced any new vision symptoms. The glaucoma medication was tapered and, given that the location of the toxoplasmosis chorioretinitis was limited to the superotemporal periphery, no treatment was indicated. She was followed closely by the retina specialist. The condition eventually resolved on its own. She was seen 1 year later by our eye service with a densely pigmented toxoplasmosis scar (Figure 3). She was reminded to call our clinic immediately if she notices any new spots or vision issues, and to see a retina specialist upon her return home to Brazil.

The Organism’s Life Cycle and Transition Toxoplasmosis is a disease caused by a single celled protozoan organism, Toxoplasma gondii. Toxoplasma eggs, or oocytes, formed to protect the parasite until it can reach a host and form a tissue cyst. The...

Submit your diagnosis to see full explanation.

The Organism’s Life Cycle and Transition

Toxoplasmosis is a disease caused by a single celled protozoan organism, Toxoplasma gondii. Toxoplasma eggs, or oocytes, formed to protect the parasite until it can reach a host and form a tissue cyst. The eggs are produced in cat intestines, and are shed in their feces. Oocytes can survive in the environment for long periods of time. Animals ingest the oocytes and the organism becomes encysted in the animal’s tissues. Toxoplasma is found worldwide and can cause infections in many animals, birds, and humans. The transmission occurs by many routes, including ingestion of raw or undercooked meat infected with tissue cysts, ingestion of food or water contaminated with oocytes. They can also be transmitted by ingestion of contaminated milk, eggs, and receiving contaminated blood or organ transfusions. Tissue cysts are most commonly found in the skeletal muscle, myocardium, brain, and eyes. The toxoplasma parasite can persist for long periods of time in the bodies of humans and other animals, possibly even for a lifetime. Of those who become infected, few experience symptoms because a healthy person’s immune system usually keeps the parasite from becoming active. 


When a human is infected with the protozoan parasite Toxoplasma gondii, ocular toxoplasmosis is a frequent clinical manifestation.2 For the majority, ocular toxoplasmosis involves the posterior eye. The pale lesion is often seen with peripheral pigmentation changes from the retinal pigment epithelium.2,3 OCT can be used to image ocular toxoplasmosis in living patients and demonstrate the retinal pigment epithelial (RPE) changes in the early phase.4 

Ocular toxoplasmosis can involve the retinal pigment by both thickening and splitting into new pigment cells. The new pigment cells have the possibility of becoming infected with the organism.3 The pigment deposits in this case are denser than typical, and a mild unreported self limited recurrence could explain this finding.3 OCT can be used to view the pigment layer, but the lesion is significantly characteristic enough so that additional investigation is not necessary to make the diagnosis. 

Without the pigmentation deposits, the diagnosis would be more difficult and require blood testing. Recurrences of lesions often occur near the edge of the previous lesion. The patient requires close monitoring in the early phase of the disease and then regularly throughout life. 

Risk and Prevalence

Ocular toxoplasmosis produces an inflammatory reaction of the retina and choroid which is in part related to a hypersensitivity reaction. Our patient was 27, and had a low risk lesion, as it was in the far periphery. In high T. gondii endemic regions in the US and Europe, ocular toxoplasmosis is the most frequent cause of posterior uveitis, presenting with a unilateral chorioretinal lesion associated with inflammation of the vitreous. A high prevalence of ocular toxoplasmosis has been reported in Africa and in South America, where our patient is from.5,6 

Multiple atypical presentations have also been reported worldwide, and severe inflammation is seen in immunocompromised patients and older patients. In general, during long term follow ups, recurrences are common. Some patients may have multiple attacks. The events may be unilateral or bilateral.3 

Vision Loss, Recurrences, and Treatment

Ocular toxoplasmosis events in immunocompromised patients, older patients, or those events that involve the macular or optic nerve may cause significant vision loss and require systemic drug treatment.3,7 Ocular toxoplasmosis in adult life was, at first, presumed to be the recurrence of a congenitally acquired infection, but more recent findings report that acquired infections account for a larger portion of the general and ocular involvement events.7 The CDC has reported that Toxoplasmosis is considered a “neglected parasitic infection” in the United States, and has been targeted for public health action.8

The classic lesion and case history in younger individuals is similar to the case presented. Ocular toxoplasmosis may be self-limited in some patients. The goal of treatment is to arrest the multiplication of the organism during the active phase of the lesion and to minimize any potential damage to the retina and optic nerve. The decision to treat should be based on several factors such as involvement of the macular or optic nerve, as mentioned above. Small peripheral lesions with localized exudation may be observed initially. Many recurrences of peripheral events have the potential for development of sight-threatening issues. Treatment may be recommended in these cases, because each episode may cause severely elevated IOP and damage the optic nerve, or cause macula issues.3 

In pregnancy, the infection can be passed from mother to fetus via placental circulation resulting in congenital infections. Intravitreal injections of clindamycin are recommended, when indicated, for pregnant patients.9

Historically, “classic treatment” is a combination of drug combinations (pyrimethamine and sulfadiazine). Several other systemic drug combinations are also popular. Some current popular systemic treatments are a combination of sulfamethoxazole and trimethoprim, or azithromycin. Oral corticosteroids should not be employed until control of the infection is in place. Classic treatment, or other systemic treatments, are not without risk and require regular monitoring. All current treatment combinations result in inhibition of the proteins needed for the parasite to develop and replicate. Patients under systemic treatment should be monitored with periodic complete blood counts for abnormal findings related to the systemic drug treatments. Sulfadiazine is also monitored for intolerance or allergy to sulfa drugs. Other systemic drug combinations of drugs may be preferred, but all require careful monitoring and follow up for any adverse drug reactions. Current drug treatments do not kill the organism, but are attempts to limit repeat events.7 

Drug treatment vs monitoring of the patient, represents the classic risk vs benefit relationship. Monitoring the patient closely for the first few months, is recommended in patients with low risk lesions, such as our patient. Treatment is indicated if repeat events occur, or other lesions form in the central fundus area or optic nerve. Our patient showed no reported signs of recurrences elsewhere, when followed by the retinal specialist, or later, during our watch.


  1. McAuley JB. Congenital Toxoplasmosis. J Ped Infect Dis Soc. 2014;3(S1);S30–S35. doi:10.1093/jpids/piu077
  2. Khan K, Khan W. Congenital toxoplasmosis: An overview of the neurological and ocular. Parasitology International. 2018;67(6):715-721. doi:10.1016/j.parint.2018.07.004
  3. Butler NJ, Furtado JM, Winthrop KL, Smith JR. Ocular Toxoplasmosis ll: Clinical features, pathology and management. Clin Exp Ophthalmol. 2013;41(1):95-108. doi:10.1111/j.1442-9071.2012.02838.x
  4. Monnet D, Averous K, Delair E, Brézin AP. Optical coherence tomography in ocular toxoplasmosis. Int J Med Sci. 2009;6(3):137-138. doi:10.7150/ijms.6.137 
  5. Rouatbi M, Amairia S, Amdouni Y, et al. Toxoplasma gondii infection and toxoplasmosis in North Africa: a review. Parasite. Published online February 15, 2019. doi:10.1051/parasite/2019006.
  6. de Lima Bessa G, Wagner de Almeida Vitor R, Dos Santos Martins-Duarte E. Toxoplasma gondii in South America: a differentiated pattern of spread, population structure and clinical manifestations. Parasitol Res. 2021;120(9):3065-3076. doi:10.1007/s00436-021-07282-w. Epub 2021 Aug 14.
  7. Ozgonul C, Besirli CG. Recent developments in the diagnosis and treatment of ocular toxoplasmosis. Ophthalmic Res. 2017;57(1):1-12. doi:10.1159/00049169
  8. Parasites – Toxoplasmosis (Toxoplasma infection). Centers for Disease Control and Prevention (CDC). https://www.cdc.gov/parasites/toxoplasmosis/index.html. Updated September 5, 2018. Accessed May 16, 2022.
  9. Rajapakse S, Shivanthan MC, Samaranayake N, Rodrigo C, Fernando SD. Antibiotics for human toxoplasmosis: a systematic review of randomized trials. Pathog Glob Health. 2013;107(4):162–169. doi:10.1179/2047773213Y.0000000094