Infectious Mononucleosis vs Toxoplasmosis
Infectious Mononucleosis and Toxoplasmosis are easy to mix up on the boards. Here's a side-by-side comparison — presentation, workup, imaging, and first-line treatment — drawn from our full outlines.
Infectious Mononucleosis vs Toxoplasmosis at a glance
- Infectious Mononucleosis: Acute viral syndrome caused by Epstein-Barr virus — fever, pharyngitis, posterior cervical lymphadenopathy, fatigue, and atypical lymphocytosis.
- Toxoplasmosis: Obligate intracellular protozoan infection (Toxoplasma gondii) — usually asymptomatic, but causes severe congenital disease and CNS lesions in immunocompromised hosts.
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Side-by-side comparison
| Feature | Infectious Mononucleosis | Toxoplasmosis |
|---|---|---|
| At a glance | Acute viral syndrome caused by Epstein-Barr virus — fever, pharyngitis, posterior cervical lymphadenopathy, fatigue, and atypical lymphocytosis. | Obligate intracellular protozoan infection (Toxoplasma gondii) — usually asymptomatic, but causes severe congenital disease and CNS lesions in immunocompromised hosts. |
| Classic presentation | An adolescent with sore throat, fatigue, posterior cervical adenopathy, and a diffuse maculopapular rash after a course of amoxicillin given for presumed strep is EBV until proven otherwise.; Prodrome (1-2 weeks): malaise, low-grade fever, headache, anorexia; Classic triad: fever, exudative pharyngitis (often with palatal petechiae),… | AIDS patient with CD4 <100, headache, focal neuro deficit, and multiple ring-enhancing brain lesions on MRI in the basal ganglia or gray-white junction — toxoplasmosis until proven otherwise. Congenital infection: diffuse intracranial calcifications (vs. periventricular in CMV).; Immunocompetent: usually asymptomatic; minority develop… |
| Workup / key labs | Clinical syndrome + positive heterophile antibody OR positive EBV VCA IgM with negative EBNA-1 IgG.; CBC with differential: lymphocytic predominance with ≥10% atypical lymphocytes (Downey cells); Heterophile antibody (Monospot) — positive in ~85% of adolescents/adults; may be falsely negative in the first week and in young children (<4… | Clinical syndrome + serology/PCR + imaging. CNS toxoplasmosis in HIV often diagnosed empirically with response to therapy (2-week trial); biopsy if no improvement.; Toxoplasma IgG (lifelong) and IgM (acute; IgM can persist >1 year); IgG avidity (high avidity excludes recent infection — useful in pregnancy); PCR — amniotic fluid… |
| Imaging | Abdominal ultrasound only if splenic enlargement clinically suspected and would change activity counseling (most evidence does not support routine imaging) | MRI brain with contrast: multiple ring-enhancing lesions with surrounding edema, predilection for basal ganglia and gray-white junction; CT (if MRI unavailable): hypodense lesions with ring enhancement; Fetal ultrasound: hydrocephalus, intracranial calcifications, IUGR, hepatosplenomegaly; Funduscopic exam for chorioretinitis |
| First-line treatment | Supportive care: hydration, NSAIDs/acetaminophen, rest, throat lozenges/saltwater gargles; Avoid contact sports/heavy exertion for at least 3 weeks (and until splenomegaly resolves) due to splenic rupture risk; Avoid amoxicillin/ampicillin — high rate of maculopapular rash (immune-mediated, not true allergy) | Acute acquired in immunocompetent host: typically no treatment unless severe or visceral disease; Ocular toxoplasmosis: pyrimethamine + sulfadiazine + leucovorin × 4-6 weeks; corticosteroids if vision-threatening; CNS toxoplasmosis (HIV/immunocompromised):; • Pyrimethamine 200 mg load then 50-75 mg PO daily + sulfadiazine 1-1.5 g PO QID… |
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