A 35-year-old immunocompetent patient from endemic Brazil presents with unilateral floaters, photophobia, and decreased vision for 10 days. Fundoscopy reveals a hyperpigmented chorioretinal scar with an adjacent white-yellow fluffy focal chorioretinitis and overlying vitritis ("headlight in the fog" appearance). The lesion is located 2 disc diameters from the macula. Serology shows positive IgG and negative IgM for Toxoplasma gondii. The structure marked **A** in the diagram represents the standard first-line pharmacological approach for this sight-threatening lesion. Which of the following best describes the rationale for adding the corticosteroid component in this regimen?
A. To enhance blood–retinal barrier penetration of sulfadiazine
B. To prevent bone marrow suppression from pyrimethamine
C. To reduce intraocular inflammation and prevent macular edema while antibiotics eliminate the parasite
D. To directly kill Toxoplasma tachyzoites in the retina
Explanation
Why "To reduce intraocular inflammation and prevent macular edema while antibiotics eliminate the parasite" is right
The classic triple therapy for ocular toxoplasmosis (pyrimethamine + sulfadiazine + leucovorin) targets the parasite directly. Oral prednisolone 0.5–1 mg/kg is added 24–48 hours after antibiotics are initiated specifically for sight-threatening lesions (macular, juxtafoveal, juxtapapillary, or large lesions with significant vitritis) to suppress the inflammatory response triggered by parasite death and tissue damage. This prevents complications such as cystoid macular edema and macular scarring while the antimicrobials eliminate the organism. The juxtamacular location in this case qualifies as sight-threatening, making corticosteroid addition essential (Kanski 9th ed; AAO Uveitis PPP 2024).
Why each distractor is wrong
To directly kill Toxoplasma tachyzoites in the retina: Corticosteroids have no direct antiparasitic activity. Pyrimethamine and sulfadiazine are the agents responsible for killing tachyzoites; prednisolone is purely anti-inflammatory.
To prevent bone marrow suppression from pyrimethamine: Folinic acid (leucovorin) is the agent that prevents pyrimethamine-induced bone marrow suppression by providing an alternative folate pathway. Prednisolone has no role in this protective mechanism.
To enhance blood–retinal barrier penetration of sulfadiazine: Corticosteroids do not enhance antibiotic penetration into the retina. The blood–retinal barrier penetration of sulfadiazine is determined by its pharmacokinetic properties, not by concurrent corticosteroid use.
High-YieldNEET PG
Prednisolone in ocular toxoplasmosis is added 24–48 hours after antibiotics to reduce inflammation in sight-threatening lesions; it does not kill the parasite and must never be given before antimicrobial therapy begins.
