Case Presentation:

A 25‐year‐old white man presented with a fever of 100.4°F, pharyngeal erythema lymphadenopathy, and flu‐like symptoms. Laboratory evaluations revealed lymphocytosis, monocytosis, neutropenia, and abnormal liver enzymes. Given his clinical picture and these laboratory values the patient was diagnosed with Infectious mononucleosis. Over the course of the following week, the patient continued to worsen despite hospitalization and supportive therapy. Further serology was taken to confirm the diagnosis and revealed that aVCA IgM was negative for EBV. Further studies reported that antibodies to CMV IgM and IgG were negative as were serology tests for hepatitis A, B, and C and HIV. Ophthalmologic examination revealed multiple yellow‐white patches with indistinct margins and antibodies for Toxoplasma gondii IgM were positive. The diagnosis of toxoplasmosis was confirmed and the patient was treated with pyrimethamine and sulfadiazine. He made a full recovery.


Our case highlights the importance of a thorough physical exam and a systematic approach to patients who present with nonspecific symptoms such as muscle aches, fatigue, and lymphadenopathy termed “mononucleosis‐like syndrome.” IM‐like syndromes are independently associated with fever lasting longer than 7 days, lymphadenopathy, elevated liver enzymes, and lymphocytosis ≥ 40% of white blood cells. The causative pathogens in patients presenting with IM‐like syndrome include CMV, HIV, HAV, HBV, HCV, HEV, HHV6, parvovirus B19, Rubella virus, secondary syphilis, cat‐scratch disease, Chlamydia psittaci, and Toxoplasma gondii and these must be systematically ruled out in a patient who is EBV negative. The pathophysiology that leads to this nonspecific symptom development is similar for all of these infections; IL‐12 is released early in infection and potentiates the production of IFN‐γ by NK cells and T cells. Proinflammatory cytokines and macrophages respond directly to parasite antigens by producing IL‐12 and TNF‐α perpetuating this inflammatory cycle until the inciting pathogen is controlled. Toxoplasmosis is caused by infection with an obligate intracellular protozoan that passes from animal reservoirs to humans. Misdiagnosis is common given that symptoms of the infection mirror those of common pathogens and otherwise healthy immune systems usually present with these indiscriminate symptoms. Patients with normal immune systems may develop serious eye infections if misdiagnosed and those with compromised immune systems can develop life‐threatening complications such as seizures and encephalitis which may prove fatal in those with AIDS. Furthermore, relapse is a persistent concern for immunocompromised people with toxoplasmosis hence prompt diagnosis and treatment is paramount.


Thorough physical exam and a systematic approach to patients who present with nonspecific symptoms of IM‐Like syndrome are imperative to appropriate therapy.