7,8 Since our patient immigrated to Germany only 2 years before initial diagnosis, and has never visited southern Germany’s AE endemic areas, it is suggestive that he acquired the disease in Siberia, a highly endemic region. Surveillance systems are not standardized in most endemic countries. In some countries surveillance does not exist at all, therefore incidence rates might be strongly underestimated. The annual global incidence is estimated to be

approximately 18,235 cases (0.26/100,000), of which 16,629 [(91%); 1.24/100,000] have been described in learn more China, and 1606 cases outside China.9,10 Globalization and increased immigration of people from highly endemic to non-endemic areas could potentially raise the number of cases in non-endemic areas.11 Epigenetic inhibitor However, the exposure risk of the usual, short-term traveler to acquire AE is minimal; no cases have been reported so far. Cerebral AE as a differential diagnosis needs to be considered in patients presenting

with neurological symptoms, cerebral lesions, eosinophilia of unknown origin, and who live in or are returning from endemic areas. In endemic areas, regular serological testing and imaging procedures would be important tools for early detection. In general, positive serology does not necessarily confirm diagnosis as antibody titers can also be interpreted as serum residuum titers, ie, in our

patient from hepatic AE. Serology is positive in up to 80% of cases; cross reaction with other helminths is possible. However, recent advanced serology using recombinant antigens such as RecEm18 appears to detect more than 95% of active AE with almost no cross reaction with non-echinococcus diseases.12 Histopathological diagnosis from Teicoplanin tissue specimen is the gold standard but not available universally. In addition to that, it is especially difficult to obtain from the brain. A polymerase chain reaction has been established in specialized laboratories. Molecular diagnostic from tissue specimen might be helpful in selected cases. The treatment of cerebral AE is often difficult: surgical removal, followed by at least 2 years, sometimes life-long chemotherapy is the standard therapy. Treatment with benzimidazoles is the preferred option.4,13 In inoperable disease, chemotherapy with anthelmintic medication is the only treatment shown to be potentially effective, but is usually palliative.13 Because of its better resorption ABZ, compared to mebendazole, is the treatment of choice. Serum levels of ABZ and its active metabolite ABZ-sulfoxide should be monitored for dose adjustments and thus the prevention of side effects and disease progression. Failure to reach therapeutic drug levels or eradicate viable lesions remains a problem, as shown in our patient.