NEWS & EVENTS
Retinal Review, Issue 74
Written by Danielle Strauss, MD
A 25-year-old woman was referred for evaluation for blurred vision in the right eye. She had recently given birth to a baby girl and but was not breast-feeding. She reported pain in the right eye, sensitivity to light and black spots in her vision for 2 to 3 weeks. She had no significant medical or surgical history. She also reported feeling “pressure” in the right eye. On examination, visual acuity was 20/70 in the right eye and 20/20 and the left eye. IOP was 21 OD and 14 OS. On the anterior exam, the patient had mild conjunctival injection, and 2+ cells and flare in the anterior chamber in the right eye. The left eye anterior segment examination was within normal limits. On DFE there was a hazy view to the retina with vitritis. There was evidence of chorioretinal scars along the superior arcade with an adjacent white lesion representing active retinitis. The DFE and the left eye was within normal limits
SD – OCT of the right eye showed vitritis, incomplete PVD, and no CME. The SD-OCT of the macula showed normal macular contour and no vitritis.
The differential diagnosis in this patient who is presenting with retinochoroiditis in her right eye is broad. It includes both infectious and noninfectious causes. Infectious causes of retinochoroiditis can include tuberculosis, syphilis, or toxoplasmosis. Viruses may also cause it, including cytomegalovirus and herpes simplex virus. Noninfectious causes include Behcet syndrome, Vogt Koyanagi Harada disease, or autoimmune conditions.
In this case, the patient had many classic findings associated with toxoplasmosis uveitis. Toxoplasmosis is the most common cause of infectious retinochoroiditis in immunocompetent people, and it accounts for approximately 90% of all focal necrotizing retinitis in general. Toxoplasma gondii is an intracellular protozoa parasite. Toxoplasma is widespread throughout the world with rates of infection highest in tropical regions of the globe. Congenital transmission is possible, but more commonly, transmission occurs by ingesting oocysts that are found in contaminated food, raw meats, raw eggs, unpasteurized milk for unwashed vegetables. Toxoplasma can also be transmitted through contact with cat feces.
Systemic Toxoplasma infection in most immunocompetent patients is asymptomatic and usually self-limiting. Systemic infection in immunocompromised patients or in babies can be much more severe.
The typical clinical presentation of ocular toxoplasmosis depends on the location and severity of the retinochoroiditis. Typically there is a new, unilateral, white/yellow retinal lesion with adjacent old pigmented chorioretinal scar. There is focal overlying vitritis by the lesion. There may be anterior chamber spillover of the inflammation, and 10 to 20% of patients may have elevated IOP. Decreased vision may occur as a result of the vitritis or if there is macular involvement. In immunocompromised patients, such as those with HIV, there may be a typical features such as large confluent areas of infection or bilateral lesions. Neuroretinitis is another atypical manifestation of toxoplasmosis in which edema the optic nerve head is seen.
When the diagnosis is in doubt, and anterior chamber paracentesis and sampling of the aqueous may be performed which can be tested for Toxoplasma with PCR (polymerase chain reaction) testing. In atypical cases HIV testing should be considered.
In most cases, toxoplasmosis uveitis can be self-limiting and observation only can be considered. However, systemic treatment should be considered in the following instances: optic nerve head involvement, severe vitreous inflammation, loss of more than two lines visual acuity, macular lesion, any lesion in an immunocompromised host, persistent inflammation for more than one month, any case with macular edema.
The goal of treatment is to minimize damage to the retina and to stop the proliferation of them parasite.
The “classic therapy” for treatment of toxoplasmosis uveitis consists of pyramethamine and sulfadiazine plus oral corticosteroids. However, these drugs have unfavorable side effect profiles and are not readily available at pharmacies. The most common therapy, for patients who do not have a sulfa allergy, is treatment with trimethoprim/sulfamethoxazole (Bactrim) with supplemental oral corticosteroids. Another drug option is azithromycin. Anterior segment inflammation is treated with topical prednisolone acetate in a cycle pleaded can be used as needed. Elevated IOP can be treated with anti-glaucoma medications.
In this case, the patient was started on a 6 week course of double strength Bactrim and prednisone (0.5mg/kg) was added two days after starting the Bactrim. The patient was also placed on topical prednisolone and cyclogyl.
On follow-up two weeks later, it was evident that the vitritis was resolving, the patient was slowly tapered off prednisone.
On the most recent follow-up, patient reports vision is significantly improved. Visual acuity returned to 20/20 in the right eye and IOP was 14. DFE revealed that the new toxoplasmosis lesion had become inactive and formed a chorioretinal scar.