BSE- The European Perspective(30分)
○Anne Balkema-Buschmann, Martin H. Groschup (Friedrich-Loeffler-Institut, Institute of Novel and Emerging Infectious Diseases)
As an introduction to this presentation, a short overview on the organization, the history and the future perspectives of the Friedrich-Loeffler-Institut will be given.
After the first cases of bovine spongiform encephalopathy (BSE) in Great Britain in the late 1980ies, a large epidemic developed in this country resulting in more than 180.000 notified cases, with the peak of up to 1000 new cases per week during 1991-1994. A few years later in 2000/2001, increasing numbers of BSE cases were detected in other European countries, leading to the implementation of BSE eradication measures according to EU regulation 999/2001. These included rapid testing of healthy slaughtered cattle above a certain age limit, identification and disposal of specified risk materials, and prohibition of the feeding of ruminant proteins to farmed animals. The combination of these three measures was very successful, as the oral infection of cattle was efficiently stopped, resulting in a clear decrease of notified cases from 2005 onwards. In 2015, only 4 BSE cases were notified in Europe plus one case in Canada. This very positive development has partly been compromised by the detection of so-called atypical BSE cases since 2004, adding up to more than 100 cases worldwide to date. Since these cases occur mostly in older cattle and independently of the classical BSE situation in a country, a spontaneous origin of these cases is generally assumed. During the last years, the BSE eradication measures have been reduced step by step, in accordance to the actual BSE situation. Despite the generally very positive situation, individual cases of classical BSE have been notified in younger animals (< 6 years) recently in the UK, Ireland, France and Canada. The etiology of these cases is currently under investigation.
Chronic Wasting Disease Research in USD(30分)
○Dr. Justin Greenlee (Virus and Prion Research Unit, National Animal Disease Center, Agricultural Research Service, United States Department of Agriculture)
Two works were designed to better understand the increased number of cases and expanded geographic range of CWD, a naturally-occurring, fatal prion disease of cervids: (1) oral transmission of scrapie to white-tailed deer and (2) horizontal transmission of CWD to non-inoculated reindeer. The purpose of the first study was to determine susceptibility of white-tailed deer (WTD) to the agent of sheep scrapie and to compare the resultant PrPSc to that of the original inoculum and CWD. We inoculated WTD by a natural route of exposure (concurrent oral and intranasal (IN); n=5) with a US scrapie isolate. All scrapie-inoculated deer had evidence of PrPSc accumulation. PrPSc was detected in lymphoid tissues at preclinical time points, and deer necropsied after 28 months post-inoculation had clinical signs, spongiform encephalopathy, and widespread distribution of PrPSc in neural and lymphoid tissues. Western blotting (WB) revealed PrPSc with 2 distinct molecular profiles. WB on cerebral cortex had a profile similar to the original scrapie inoculum, whereas WB of brainstem, cerebellum, or lymph nodes revealed PrPSc with a higher profile resembling CWD. Homogenates with the 2 distinct profiles from WTD with clinical scrapie were further passaged to mice expressing cervid prion protein and intranasally to sheep and WTD. The second passage to WTD is still ongoing, but deer in both inoculation groups are positive for PrPSc by rectal mucosal biopsy. In summary, this work demonstrates that WTD are susceptible to the agent of scrapie, two distinct molecular profiles of PrPSc are present in the tissues of affected deer, and inoculum of either profile readily passes to deer.
The aims of the second study were to 1) investigate the transmission of CWD from white-tailed deer (Odocoileus virginianus; CWDwtd), mule deer (Odocoileus hemionus; CWDmd), or elk (Cervus elaphus nelsoni; CWDelk) to reindeer via the intracranial route, and 2) to assess for direct and indirect horizontal transmission to non-inoculated sentinels. Three groups of 5 reindeer fawns were challenged intracranially with CWDwtd, CWDmd, or CWDelk. Two years after challenge of inoculated reindeer, non-inoculated negative control reindeer were introduced into the same pen as the CWDwtd inoculated reindeer (direct contact; n=4) or into a pen adjacent to the CWDmd inoculated reindeer (indirect contact; n=2). Intracranially challenged reindeer developed clinical disease from 21 months post-inoculation (months PI) and PrPcwd was detected in 5 out of 6 direct or indirect contact reindeer. We have shown that reindeer are susceptible to CWD from various cervid sources and can transmit CWD to naïve reindeer both directly and indirectly.