Case Presentation:

A 48‐year‐old white female with no previous chronic disease presented with a 2‐week history of constitutional symptoms including fever, rhinorrhea, and malaise. After failure of the initial therapeutic trials, she underwent a complete workup to rule out infectious, inflammatory, or neoplastic diseases. In addition to conventional studies (e.g., chest x‐ray and cultures), numerous diagnostic tests including antinuclear antibody, anticardiolipin antibody, antineutrophil cytoplasmic antibody, hepatitis A, B, and C serology, HIV ELISA test, and transthoracic echocardiography were performed, all with normal results. Atypical lymphocytes were detected in the peripheral blood smear. CT scan of the chest, abdomen, and pelvis revealed massive splenomegaly and multiple splenic infarcts, as well as multiple pulmonary emboli within branches of the right upper and lower pulmonary arteries. Magnetic resonance angiography (MRA) of the abdomen revealed a right renal vein thrombus (RVT) extending into the inferior vena cava. There existed abnormal flow in the splenic artery and vein as well. Although the Ebstein‐Barr virus (EBV) serology was only positive for IgG, the cytomegalovirus (CMV) serology came back positive for both IgG and IgM. with CMV DNAas high as 4616 copies/dL. The diagnosis of CMV related infectious mononucleosis (IMN) complicated with TEC (pulmonary embolism and RVT) was made in the absence of any laboratory evidence for a congenital hypercoagulable state. Anticoagulation therapy associated with conservative management resulted in resolution of the symploms, splenomegaly, and disappearance of CMV IgM antibody.


CMV infection has been associated with thrombosis in immunocompromised patients, including those infected with HIV and transplant recipients. In addition, there have been case reports of thrombotic events in immunocompetent hosts with CMV infection. The exact nature of the procoagulant effect of CMV is not clear, but it is thought to be related to endothelial inflammation, vasculitis, and occlusive vascular ischemia.


Similar to severe systemic infections in immunosuppressed patients, a mild viral systemic infection, such as CMV‐releted IMN, might present with TEC in an immunocompetent host. Further studies are needed to assess The potential role of such mild systemic infections as an unrecognized cause of TEC in this setting. Meanwhile, inpatient providers would be juslified to maintain a high index of suspicion for possible thromboembolic events in patients with identified acute CMV infection.

Author Disclosure:

M. Sattari, none.