Collaborative Case #005: Things that Bug the Retina
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Case Presentation
A 29-year-old White male was referred to my practice to rule-out a posterior vitreous detachment (PVD) OS. His symptoms included “very fuzzy vision with cloudy floaters” in his left eye last one and a half weeks. He had no prior medical or ocular conditions, had never worn glasses, did not take any medications, had no known allergies and never smoked. The patient also reported no known ocular family history, but did note that his grandparents had a history of diabetes.
His uncorrected VAs were 20/20 OU. Extraocular movements, primary gaze, and confrontation fields were normal. His pupils were equal, round, reactive to light, and had negative afferent pupillary defect. His IOPs were 14 mm Hg OD and 15 mm Hg OS. Anterior segment and slit-lamp examination was only remarkable for few keratic precipitates and trace cells in the anterior chamber OS (Figure 1).


OCT showed slight lifting of the posterior vitreous cortex with subhyaloid accumulation of inflammatory cells (Figure 2; blue arrow) in the macular area, while the macula remains normal.
Increased internal reflectivity and retinal thickness was noted in the involved area, with thickening of the inner retina and detachment of the posterior hyaloid and vitreous cell over the infected area. There is shadowing of the underlying choroid; however, the choroid has also shown increased thickening in the diseased area as compared with its adjacent area (Figure 2; boxes). These are biomarkers for retinochoroiditis.
The patient was prescribed antibiotics and was sent for a laboratory workup for posterior uveitis, which included titers for Toxoplasmosis gondii (T. gondii).
At the 2-weeks follow-up, the patient indicated good adherence and tolerance to oral trimethoprim- sulfamethoxazole 80 mg/400 mg twice daily and significant improvement of his presenting symptoms. His VA remained 20/20 OU. Fundus and OCT examination showed signs of improvement.
The fundus examination is remarkable for decreased whitening of the lesion, while OCT showed signs reduced internal reflectivity, decreased retinal and choroidal thickness, and overlying vitritis. Retinal derangement and early necrosis in the area affected by the offending organism is also visible (Figure 3).

The patient was instructed to remain on the oral medication until further follow-up.
Epidemiology
T. gondii is an infection that's common worldwide. In the United States, the Centers for Disease Control estimates that 11% of the population 6 years of age and older and in some areas of the world, as high as 60% of the local population, are affected by this protozoan infection.1 This is not considered a person-to-person infection; most commonly, it is a foodborne, then animal-to-human, and at times mother-to-child in the congenital form. Feline play the key role in the spread of toxoplasmosis. They become infected by consuming small, infected animals, such as rodents and birds.
Systemic Symptoms
Most infected individuals don't not have any symptoms and are unaware of the infection. Some may experience flu-like symptoms including fever, swollen lymph nodes, headache, malaise, muscle aches, and skin rash.2
Pathophysiology
After T. gondii settles in the small intestine, its tachyzoites travel via blood or lymphatic systems to remote sites.3 The parasite proliferates once it reaches the retina, inviting and destroying the nearby host cells, which results in the primary lesion being notable clinically.4
The host immune system then restricts, causing scar formation. At times, the scar can be reactivated at the same site or in a form of a satellite lesion in another area.4
This result is what is known as toxoplasmosis retinochoroiditis or necrotizing chorioretinitis.
Clinical Presentation and Diagnosis
In the acute phase, localized areas of retinal whitening with overlying vitritis can be detected clinically and/or with imaging such as OCT or OCT angiography.4,5 Retinal vasculitis, as well as arterial occlusion, can be seen typically in or near the infected region.4 In inactive phase pigmentation of the chorioretinal lesions are noted and in recalcitrant and recurrent situations a combination of active and inactive lesions can be observed. Associated nongranulomatous iridocyclitis can also be present.
Toxoplasmosis retinochoroiditis is the most common infectious retinitis; however, differential diagnosis includes other infectious etiology. These include acute retinal necrosis; which is thought to have a herpetic etiology, CMV retinitis, and fungal cases.
Treatment
Small, nonmacular lesions with minimal vitritis can be monitored closely with no intervention. Traditional treatment is with a combination of sulfonamides, such as sulfadiazine and pyrimethamine, an antiparasitic agent also used for malaria. There is a commercially available combination of sulfafadaxine and pyrimathamine (Fansidar, Roche Laboratories).4-6 Folinic acid is prescribed concurrently to reduce pyrimthamine-related hematologic adverse reactions. Alternative treatments include sulfamethoxazole/trimethoprim 800 mg /160 mg with or without azithromycin which can improve the effect.7 Oral or intravitreal clindamycin can be considered in cases of allergy to sulfa or lesions involving the macula or the optic nerve.8
Visual prognosis of ocular toxoplasmosis depends on the size and location of primary or secondary lesions. It will also improve with timely diagnosis and treatment of the vision threatening cases.
IMPORTANT TAKEAWAYS
Ocular toxoplasmosis is a common condition that is relatively easy to diagnose. Timely diagnosis and management often results in good prognosis. Optometrists need to keep this diagnosis in their checklist of patients who present with a sudden onset of “floaters” and particularly “foggy” vision.
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ABOUT THIS SERIES
On the path from initial diagnosis to severe disease management, patients may encounter a number of eye care providers. The Collaborative Care Case Series was developed, with guidance from William Trattler, MD, and Diana Shechtman, OD, FAAO, to challenge clinicians' understanding of diagnostic and treatment conventions and advance knowledge of all eye care providers along the continuum.
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