Ocular Toxoplasmosis

Ocular Toxoplasmosis
SYMPTOMS Decreased central vision, Metamorphopsia, Visual field loss, Floaters, Eye pain, Photophobia
SIGNS Anterior uveitis (can be granulomatous), Posterior uveitis, Posterior synechiae, Vitritis, Fluffy white or yellowish retinal lesion (typically greater than 1DD) with overlying vitreous cells (described as “headlights in a fog”) which may be adjacent to a chorioretinal scar (inactive lesion), Retinal vasculitis, Epiretinal membrane, Retinal perivascular sheathing, Branch retinal artery occlusion, Branch retinal vein occlusion, NVD, NVE, Neuroretinitis, Cystoid macular edema, Vitreomacular traction, Choroidal neovascular membrane, Preretinal hemorrhage, Subhyaloid hemorrhage, Intravitreal hemorrhage, Retinal detachment
WORK-UP Pupils, Full eye exam with dilated retinal exam, Gonioscopy, OCT analysis of the macula, OCT analysis of the optic nerve, OCT-Angiography, Fluorescein Angiography, Indocyanine Green Angiography, Fundus Autofluorescence, Fundus photos, Infrared photos, B-scan ultrasound (if unable to view the retina), Watzke-Allen test, Macular photostress test, Amsler grid
TREATMENT Give take home Amsler grid in order to monitor for change
Patient needs to use caution with any strenuous exercise or activities in the presence of retinal neovascularization
Patient should sleep with their head elevated in presence of a preretinal, subhyaloid, and/or intravitreal hemorrhage
Consider discontinuing or lowering the dosage of any blood thinners in the presence of vitreal and/or retinal hemorrhaging (needs to be discussed with PCP)
If the patient presents with active lesions in the peripheral retina with little to no symptoms, the patient just needs to be monitored
If patient presents with an anterior uveitis with or without posterior synechiae, the patient should be started on a topical steroid (Prednisolone acetate or Durezol) and a topical cycloplegic (patient will most likely also have a posterior uveitis as well as other complications and will ultimately need to be treated by a retinal specialist)
Refer to a retinal specialist ASAP for further evaluation and treatment if the patient presents with the following: An active lesion is in the posterior pole, Involvement of the macula and optic nerve, Vision loss of 2 lines or more, Active lesions are associated with a severe vitritis, Active lesions are present and patient is immunocompromised or pregnant, Active lesions are present and patient is monocular, The presence of NVD/NVE/Choroidal neovascular membrane/Cystoid macular edema/Preretinal hemorrhage/Subhyaloid hemorrhage/Intravitreal hemorrhage/Retinal detachment
Treatment usually consists of Pyrimethamine, Sulfadiazine, Clindamycin, and Prednisone or Bactrim and Prednisone (Prednisone is typically started 2-3 days after the antibiotic treatment). Treatment usually lasts for 4-6 weeks
The combination of Bactrim and Prednisone works best to prevent recurrence
FOLLOW-UP If patient is just being monitored because there are active lesions in the peripheral retina with little to no symptoms, that patient should be seen back once a month until active retinal lesions are no longer active
Once the patient's ocular toxoplasmosis is treated by the retinal specialist and the ocular inflammation is no longer active with a stable retina/macula/optic nerve, the patient should be seen back every 6 months
ADDITIONAL LAB | TESTS Sabin-Feldman dye test, Indirect fluorescent antibody testing, IgG titers, IgM titers, Polymerase chain reaction
ETIOLOGY Occurs due to ocular infection from the parasite Toxoplasma gondii
DIFFERENTIAL DX Ocular tuberculosis, CMV retinitis, Presumed ocular histoplasmosis, Ocular toxocariasis, Ocular syphilis
NOTES Toxoplasmosis is the most common cause of an infectious retinochoroiditis
About 24% of patients with ocular toxoplasmosis end up seeing 20/200 or worse due to scarring at the macula and/or optic atrophy
The risk of a toxoplasmosis infection is significantly greater in patients who are immunocompromised
Ocular toxoplasmosis is unlikely to reoccur the longer the time interval from the initial ocular infection (risk of recurrence is highest within the first year of the initial ocular infection)
Toxoplasmosis can be congenital (typically transferred through the placenta) or acquired (eating raw or undercooked meat, drinking contaminated water, or coming in contact with cat feces)
The classical triad of congenital toxoplasmosis is retinochoroiditis, hydrocephalus, and intracranial calcificiations
Ocular Toxoplasmosis: Fundus photo demonstrating a large chorioretinal scar at the macula secondary to a previous toxoplasmosis infection https://imagebank.asrs.org/file/272/ocular-toxoplasmosis-scar-fundus-photograph