[Lethal alveolar echinococcosis in a dog: clinical symptoms and pathology]. / Letale alveoläre Echinokokkose bei einem Hund: Klinik und Pathologie.

Epidemiological data indicate a progressing spread of the fox tapeworm in Germany. Here we report on a case of lethal alveolar echinococcosis in a dog from Brandenburg. The patient was clinically presented with abdominal distension. Ultrasonic examination revealed severe structural alterations of the liver and in a fine needle aspiration cytology larval tape worm fragments were suspected. Explorative laparotomy suggested inoperable lesions and the animal was euthanized with unfavorable prognosis. Pathology confirmed the diagnosis of hepatic echinococcosis. PCR analysis of the liver identified Echinococcus multilocularis, the so called "small fox tapeworm". The infection, reportable in Germany, is an important zoonotic disease that is transmitted by accidentally ingested tapeworm eggs shed by foxes or dogs. The prevalence between 7.6% and 16.7% in the fox population of Brandenburg is significantly lower than in the endemic regions of South and Southwest Germany, however, it is suspected to increase. This underlines the importance of a regional monitoring in domestic animals living in close contact to humans. In this regard, especially dogs should be taken into consideration as a potential definitive host and source of infection for people.

Local delivery of IL-2 reduces atherosclerosis via expansion of regulatory T cells.

OBJECTIVE: Recent studies indicate that regulatory T cells (Tregs) attenuate murine atherosclerosis. Since interleukin (IL)-2 induces Tregs proliferation, we tested the impact of L19-IL2, a fusion antibody specific to extra-domain B of fibronectin (ED-B) containing an active human IL-2 molecule, in experimental atherosclerosis. METHODS AND RESULTS: L19-IL2 or appropriate controls were given intravenously to 6 month old Western diet-fed apoE(-/-) mice on day 1, 3, and 5. Human IL-2 was detected on day 7 within atherosclerotic plaques of L19-IL2-treated mice, and magnetic resonance imaging of the plaques showed a significant adventitial gadolinium enhancement on day 7 and 13, suggesting microvascular leakage as a result of the pharmacodynamic activity of L19-IL2. Treatment with L19-IL2 significantly reduced the size of pre-established atherosclerotic plaques at the thoracic aorta (Sudan III stained area) and in the aortic root area (microscopic, morphometric analysis) on day 7 as compared to controls (L19, D1.3-IL2, NaCl) as well as compared to baseline (day 0). Tregs markers Foxp3 and CTLA4 were highly increased in plaques after L19-IL2 treatment compared to controls (p<0.01), whereas the macrophage marker Mac3 was significantly reduced (p<0.03). Co-treatment with IL-2-receptor blocking antibody PC61 abrogated L19-IL2-induced plaque reduction compared with IgG control (p<0.03). CONCLUSION: L19-IL2 delivers functional IL-2 to pre-established atherosclerotic plaques of WD-fed apoE(-/-) mice resulting in significant plaque size reduction mediated by local Tregs.