Alveolar echinococcosis in the 21st century: An opportunistic infection?
Résumé
Increased susceptibility of experimental animals with immune suppression to alveolar echinococcosis (AE), due to Echinococcus multilocularis infection, has been known for more than 30 years, as well as the fast progression of residual AE lesions in patients with liver transplantation. However, occurrence of AE in patients with acquired immune suppression has been published as isolated cases only from the beginning of the 21st century. Based on the French Registry of Alveolar Echinococcosis cases (FrancEchino), a systematic study of AE cases in immunosuppressed patients, patients with AIDS, with cancer and malignant hematological disorders, with chronic inflammatory diseases, and with organ transplantations, has been performed. This study has confirmed the significant increase of AE cases in patients with immune suppression since 2000, compared to previous years, and of the percentage of such cases among all French AE patients, thus giving AE the status of 'opportunistic infection'. AE is most often an incidental finding in patients with a follow-up for the underlying disease. AE diagnosis is generally delayed and the treatment often erroneous because of misleading diagnostic findings, especially in patients with cancer. When the patients are symptomatic, unusual acute symptoms that simulate a liver abscess may be seen; these presenting symptoms, as well as more frequent negative serology and unusual imaging findings than in patients without immune suppression contribute to delayed diagnosis. Usual therapeutic strategy nevertheless applies to AE in immunosuppressed patients, with complete surgical resection of AE lesions whenever possible, anatomically and in the context of the underlying disease, and long-term administration of albendazole in non-operable patients. In such cases, albendazole efficacy is often excellent and fast; however, adverse effects of albendazole seem more frequent than in other patients. Complementary studies are necessary to understand whether AE occurrence in immunosuppressed patients is due to newly acquired infection or to the reactivation of dormant microscopic lesions.