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We report a case of Echinococcus multilocularis infection of the pericardial cavity that resolved under a 4-year parasitostatic treatment with albendazole.
A 30-year-old man was admitted in March 1998 because of a pericardial mass. He had never traveled out of France and lived in Paris suburbs. In January 1997, he was referred for basal right lung pain. Blood tests showed a C-reactive protein level of 321 mg/L and a high eosinophil count of 770/mm3. Thoracentesis showed a protein- (60 g/L) and cell-rich (2370 cells/mm3) right pleural effusion with 19% eosinophils. Heart ultrasonography and computed tomographic (CT) scan showed a necrotic pericardial mass (57 × 42 mm) that compressed right cavities. A partial surgical excision of the pericardial mass revealed a granulomatous inflammation with a few giant cells and central noncaseous eosinophil necrosis. Cultures for Mycobacterium tuberculosis were negative; nevertheless, antituberculous treatment was begun in December 1997. In March 1998, clinical examination and a large blood test panel were unrevealing. Serology of echinococcosis, using an E. granulosus antigen, was positive, with one blurred arch on immunoelectrophoresis and an optical density of 0.46 (n <0.18) using enzyme-linked immunosorbent assay (ELISA). Serology using an E. multilocularis (Em) antigen was highly positive, with three thin arches on immunoelectrophoresis and an optical density of 0.4 (n <0.17) using ELISA. A more specific ELISA method showed high levels of anti-Em2 immunoglobulin (Ig) G antibodies. A CT scan (Figure 1, A) showed a growing pericardial mass (10 × 5 × 5 cm). The liver was normal. Antituberculous treatment was then switched for albendazole (800 mg/day). Two years later, the patient was symptom free, but the mass size was unchanged on CT scan. In April 2002, thorax CT scan revealed dramatic improvement (Figure 1, B). A specific anti-E. multilocularis Western blot performed in 2002 showed a significant decrease of specific bands intensity when compared retrospectively with the serum of 1998 (Figure 2). The patient is still followed as an outpatient and treated with albendazole 800 mg/day.
Echinococcosis is caused by E. granulosus (hydatid disease) and E. multilocularis (alveolar echinococcosis).
histological examination of myocardial biopsy showing usual features of E. multilocularis infection; thorax CT scan results; and serum antibodies analysis. The Em2 plus ELISA has a reported sensitivity of 97% and an overall specificity of 99% for the diagnosis of E. multilocularis infection.
In our patient, patterns obtained with a Western blot assay using E. multilocularis larval antigen were characteristic of alveolar echinococcosis and clearly distinguishable from a hydatidosis pattern (Figure 2).
Apparent absence of hepatic lesion in our patient is unusual and might be due to an initial location at the liver dome that made the metacestode grow only towards the diaphragm and the pericardium or due to a primitive pericardial location. E. multilocularis heart involvement appears exceedingly rare. In a patient with hepatic alveolar echinococcosis, pulmonary embolism was due to a right-heart parasitic clot that could be removed surgically.
To our knowledge, no case of isolated pericardial or myocardial involvement due to E. multilocularis has been reported.
In conclusion, E. multilocularis may infect the pericardial cavity without disclosable liver involvement. Sensitivity of the parasitic lesions to albendazole in this location suggests that chemotherapy should be considered when surgery is impossible or at risk. Because disease improvement may occur very late, albendazole should be pursued even when no change is disclosed over the first years of treatment. Despite objective mass regression and encouraging immunological changes, the decision to withdraw albendazole remains difficult.