A Protozoan Posterior Uveitis

A 22-year-old Black female presented complaining of blurry vision, constant black dots, and redness in her left eye that had occurred over the last week. She did not report discharge, photosensitivity, or pain. She did not have any known systemic conditions, and was wearing spectacles to correct moderate myopia and mild astigmatism. Also, the patient was not using any medications and reported no recent animal exposure, no recent travel, no fever, and no joint pain.

EXAMINATION

The patient’s entering VA was 20/20 OD and 20/25+2 OS. Her pupils, extraocular muscles, and cover test were normal. Slit lamp examination of the right eye was unremarkable. Grade 2 diffuse bulbar injection was noted in the left eye, though no discharge was seen, and there were no cells in the anterior chamber. IOP was 22 mm Hg OD and 36 mm Hg OS. The retina and optic nerve of the right eye were normal. Her left eye showed an area of focal chorioretinal inflammation 1.5 disc-diameters inferior-nasal to the optic nerve. Significant vitritis was also noted, the density of which was greatest just anterior to the inflamed area of the retina, although inflammatory cells extended to the anterior vitreous (Figure 1).

An active toxoplasmosis infection was suspected, as it was in line with the presentation of a unifocal area of inflammation.

The patient was started on a 1% corticosteroid QID in an attempt to suppress the intraocular inflammation and a 0.5% beta blocker BID in the left eye to lower her IOP. She was instructed to return 3 days later for follow up.

NEXT STEPS

As directed, the patient returned 3 days later. At this visit, she reported adherence to the prescribed medications, but there was minimal change in her symptoms. Her VA at this visit was 20/20 OD and 20/20-2 OS, and IOP was 22 mm Hg OD and 30 mm Hg OS. Although the chorioretinitis did not threaten the macula of the left eye, the patient was referred to ophthalmology for a potential workup to better determine the underlying etiology of the ocular inflammation.

The next day, ophthalmology diagnosed her with retinal vasculitis and retinitis. She was told to increase the corticosteroid to every Q2H in an attempt to arrest the inflammation, and additional IOP-lowering medications, an alpha-2 adrenergic agonist TID, and a carbonic anhydrase inhibitor TID were added to help decrease the elevated IOP. She was also prescribed 1,000 mg valacyclovir TID and oral Bactrim BID. Acute retinal necrosis secondary to herpes simplex virus (HSV) infection was on the list of potential differential diagnoses, so treatment was initiated with valacyclovir in case the lab testing ophthalmology ordered was positive for HSV. Bactrim was prescribed because this medication can be effective against toxoplasmosis.

Results from the lab testing showed positive results for HSV type 1, toxoplasmosis, and cytomegalovirus. Toxoplasmosis and acute retinal necrosis were, therefore, considered the primary differential diagnoses of our patient’s posterior uveitis at this point.

Throughout the course of the next 4 months, the patient was monitored regularly until resolution of the inflammation. Due to the unifocal nature of the lesion, the presence of toxoplasmosis antibodies, and the resolution of the condition over a few months, ophthalmology determined that the underlying etiology was most likely toxoplasmosis. There is now a unifocal scar in the previously inflamed area (Figures 2 and 3).

DISCUSSION

A recent study determined that uveitis, or inflammation of the uveal tract (iris, ciliary body, and choroid), has an incidence of 212.5 per 100,000 people in the United States.¹ The Standardized Uveitis Nomenclature divides uveitis into four types: anterior uveitis, intermediate uveitis, posterior uveitis, and panuveitis.²

In this case, the patient’s posterior uveitis was most likely due to toxoplasmosis. Posterior uveitis, one of the most common causes of blindness and low vision globally, can also result from sarcoidosis, syphilis, tuberculosis, endogenous endophthalmitis, and viruses, among other causes.

Toxoplasmosis results from an intracellular protozoan parasite (toxoplasma gondii) and can be congenital or acquired.³ The prevalence of antitoxoplasmosis gondii antibodies in individuals in North America is about 20%.⁴ One study reported the global prevalence of ocular toxoplasmosis to be 2% and the prevalence in the United States to also be 2%.⁵ The most common modes of transmission are through ingestion of infected food or water or raw or undercooked meat.³

In the eye, classic toxoplasmosis often results in a unifocal area of retinal and choroidal inflammation and vitreous inflammation.⁶ It is possible for toxoplasmosis to lead to inflammation in the anterior chamber, which can be severe. Upon resolution of the inflammation in the posterior segment, a pigmented scar will remain. One study reported differences in the features of ocular toxoplasmosis between men and women.⁷ For example, a single lesion was more likely in men, while multiple lesions were more likely in women. Additionally, lesions in women were more likely to be found in the posterior pole.

Serological testing for toxoplasmosis includes screening for immunoglobulins.^8,9 Treatment of ocular toxoplasmosis varies among affected individuals.⁴ Treatment for toxoplasmosis-induced posterior uveitis may involve both antimicrobial drugs and topical or oral steroids.⁴ The “classic therapy” for toxoplasmosis includes an antiparasitic agent, a sulfonamide antibiotic, and a systemic corticosteroid. Anterior uveitis resulting from toxoplasmosis infection may be treated with steroid eye drops.⁴

CASE CONCLUSION

The patient’s most current BCVA was 20/20 OU, and her IOPs averaged 18 mm Hg OU. Other than the chorioretinal scar in her left eye, there were no other long-term ocular comorbidities associated with this case.