gms | German Medical Science

10. Kongress für Infektionskrankheiten und Tropenmedizin (KIT 2010)

Deutsche Gesellschaft für Infektiologie,
Deutsche AIDS-Gesellschaft,
Deutsche Gesellschaft für Tropenmedizin und Internationale Gesundheit,
Paul-Ehrlich-Gesellschaft für Chemotherapie

23.06. - 26.06.2010, Köln

Accelerated larval growth of Echinococcus multilocularis in the immunodeficient host?

Beschleunigtes Larvenwachstum von Echinococcus multilocularis bei Immundefizienz?

Meeting Abstract

Suche in Medline nach

  • B. Grüner - Klinik für Innere Medizin III, CIDC, Ulm, Germany
  • G. Härter - Klinik für Innere Medizin III, CIDC, Ulm, Germany
  • K. Wahlers - Klinik für Innere Medizin III, CIDC, Ulm, Germany
  • P. Kern - Klinik für Innere Medizin III, CIDC, Ulm, Germany

10. Kongress für Infektionskrankheiten und Tropenmedizin (KIT 2010). Köln, 23.-26.06.2010. Düsseldorf: German Medical Science GMS Publishing House; 2010. DocP99

doi: 10.3205/10kit154, urn:nbn:de:0183-10kit1544

Veröffentlicht: 2. Juni 2010

© 2010 Grüner et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen ( Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.



Introduction: Human alveolar echinococcosis (AE) caused by the larval stage of the tapeworm Echinococcus multilocularis is a life threatening helminthic disease, primarily affecting the liver.

Slow larval growth with a prolonged incubation period of several years is a characteristical feature of the disease. Case reports suggest, that there are unusual presentations of AE under immunosuppressive therapy and an even more aggressive course of disease in co-infection with HIV.

We wondered if different modes of immunosuppression influence the course of AE and are associated with accelerated larval growth.

Objectives/methods: All patients treated for AE at our center from May 2005 to December 2009 were evaluated for states of immunodeficiency and the kinetics of their larval growth. Out of 200 patients we found 26 to have various states of immunosuppression in their history.

Results: 18 patients with various malignancies showed an unremarkable course of the AE.

Three patients received immunosuppressants and two patients reiceived TNF-alpha antagonist. Particularly the patients under TNF-alpha antagonists seem to have an accelerated growth of AE liver lesions.

Three women presented with AE in pregnancy, two of them seemed to have accelerated growth of their liver-lesion during pregnancy, whereas one lesion remained stable throughout pregnancy.

Discussion/conclusion: At this stage our retrospective analysis does not allow definite conclusions whether larval growth is accelerated in immunocompromised patients with AE in general.

Different kinds of immunosuppression seem to influence the dynamics of larval growth in various ways.

At our clinic 2 patients under TNF-alpha antagonist therapy developed rapidly progressing AE liver lesions. With benzimodazole- therapy these lesions stabilized.

In immunocompromised patients careful monitoring is necessary with regular follow up including imaging techniques, blood tests, and monitoring of benzimidazole therapy, including ABZ- drug levels.

But as immunosuppressive therapy is now more commonly used this needs to be evaluated further. In addition reliable criteria need to be established to assess larval growth in AE.