Search

Primary Cytomegalovirus (CMV) infection is often not suspected as a cause of fever of unknown origin (FUO) in immune-competent adults. We present a case-series of symptomatic primary CMV infection in immunocompetent adults presenting as fever of unknown origin (FUO). All patients with CMV serology tested between November 2008 and June 2016 underwent chart review. Cases were defined as those between 18 and 65 years of age with documented fever and elevated serum anti-CMV IgM. Exclusion criteria were organ specific CMV disease, positive serum anti-EBV IgM, or presence of any immunocompromising condition. Sixteen patients (69% male, mean age 42.2 ± 11.7 years) met criteria. Mean duration of illness was 4.6 ± 3.3 weeks. Common symptoms other than fever included fatigue (94%), night sweats (81%), malaise (75%), myalgias (63%), and headache (56%). Eleven patients (68.8%) had contact with young children; six (35.3%) patients had children in daycare. Twelve (75%) patients had extensive testing and multiple visits or hospitalizations prior to consulting with an infectious disease specialist. Peripheral smear was done in twelve (75%) patients and all had atypical lymphocytes. Five patients (31.3%) had a leukocytosis. Peak serum transaminases were: AST 115.25 ± 50.5 IU/L and ALT 168.38 ± 92.0 IU/L. One patient had splenic infarcts. In addition, two cases of hydrops fetalis were attributed to primary CMV infection. In summary, primary CMV infection can present as FUO in immunocompetent adults. Contact with young children in daycare may be a risk factor. Heightened clinical suspicion will promote earlier diagnosis and avoid unnecessary testing.

Background: In endemic regions, histoplasmosis is often seen in hosts with defective cell mediated immunity. We report a case of disseminated histoplasmosis in a patient with common variable immunodeficiency (CVID), a disorder mainly characterized by B cell defects., Case: A 35 year old male with CVID developed fever, headache, dyspnea and pancytopenia within few weeks of swimming in the Tennessee River. After a non-revealing initial evaluation he was transferred to a tertiary facility for fever of unknown origin, where massive splenomegaly was noted. Clinical course was complicated by hypoxia from extensive bilateral lung infiltrates requiring non-invasive ventilation. Urine and serum Histoplasma antigens were positive. He was treated with liposomal amphotericin B followed by itraconazole after clinical improvement within 48 h and discharged home by day 6. Fungal blood cultures sent on day 1 grew Histoplasma capsulatum on day 19. After 5 months splenomegaly completely resolved and he successfully completed one year of treatment with itraconazole., Conclusions: Our case highlights the significance of T cell defects in CVID. More research focusing on T cell defects in CVID is required to understand the extent of vulnerability to such intracellular pathogens in CVID.