Dr. Stephen B. Thacker Director Centers for Disease Control and Prevention′s Office of Science, Epidemiology and Laborator
Posted Apr 15 2013 9:58pm
A Family Blog for Family & Friends
On December 5th, we as a family were given unimaginable news, our father and husband, Steve, has Creutzfeldt-Jakob Disease (CJD.) We knew it was a possibility but were ever hopeful it was not this tragic news. Knowing the disease is rapidly progressive and always fatal was heartbreaking. Though we are grateful for every moment we still have left with him, seeing a man of his brilliance, sense of humor and love deteriorate is horribly painful for family, friends, and co-workers. We cannot express how thankful we are to the hundreds of well-wishes, meals, donations, prayers, thoughts, etc we have received from the community. It has been an overwhelming amount of support that we will be forever thankful for. We still have a difficult road ahead of us and we hope to keep dad’s community from CDC to basketball, to family and friends, aware of what is happening through the main website and this blog.
December 30, 2012 by teamthacker Posted in UncategorizedTagged CJD, Creutzfeldt-Jakob, Stephen B. Thacker, ThackerLeave a reply
About Team Thacker In December 2012, Stephen B. Thacker, MD, MSc, RADM/ASG (ret.), USPHS, father and husband, was diagnosed with Creutzfeldt-Jakob Disease (CJD.) Classic CJD is a human prion disease. It is a neurodegenerative disorder with characteristic clinical and diagnostic features. This disease is rapidly progressive and always fatal. Infection with this disease leads to death usually within 1 year of onset of illness.
Dr. Thacker passed away on Friday, February 15, 2013 from complications of CJD. We encourage you to visit the family website to learn more www.teamthacker.com .
Dr. Stephen B. Thacker is the Director of the Centers for Disease Control and Prevention′s Office of Science, Epidemiology and Laboratory Services (OSELS). In this role, Dr. Thacker provides critical leadership in the application of information, computer science, and technology to improve public health practice, research, and learning.
Prior to assuming this post, he was the Director of the Office of Workforce and Career Development (OWCD), where he served since June 2004. As Director of OWCD, Dr. Thacker lead the CDC program responsible for improving health outcomes by ensuring a competent and sustainable workforce through excellence and innovation in workforce and career development.
Dr. Thacker served as director of the Epidemiology Program Office (EPO), CDC in August 1989 through June 2004. As director of EPO, Dr. Thacker led the CDC program responsible for domestic and international training and consultation in epidemiology, statistics, and applied public health, as well as scientific communications.
Dr. Thacker served as acting director of the Center for Injury Prevention and Control (NCIPC) from September 1999 through November 2000. As acting director of NCIPC, Dr. Thacker led the CDC Program responsible for preventing and controlling the incidence, severity, and adverse outcomes of injury related to both violent and unintentional causes through research, public health surveillance, implementation of programs, and communications.
Dr. Thacker served as acting deputy director of CDC and deputy administrator of the Agency for Toxic Substances and Disease Registry (ATSDR) from February 1998 to October 1998. As acting deputy director of CDC, Dr. Thacker assisted leading the agency of the U.S. Public Health Service in promoting health and preventing disease, injury, and premature death. CDC’s 11 Centers, Institutes and Program Offices work closely with local, state, and other federal agencies to protect public health. As deputy administrator of ATSDR, Dr. Thacker assisted in administering the Public Health Service (PHS) agency created by the Superfund law to prevent or mitigate adverse human health effects and diminished quality of life resulting from exposure to hazardous substances in the environment.
From January 1993 to December 1994, Dr. Thacker served as acting director of CDC’s National Center for Environmental Health (NCEH). As acting director of NCEH, he led the CDC program responsible for prevention of premature death, illness, and disability due to environmental factors outside the workplace with programs developed on the foundations of epidemiology, laboratory science, and behavioral science.
He received his undergraduate degree in biochemistry at Princeton University in 1969 and his M.D. from Mount Sinai School of Medicine in 1973. He completed residency training in family medicine at the Duke University School of Medicine in 1976, and was certified by the American Board of Family Practice in 1977. At Duke, Dr. Thacker was also a Robert Wood Johnson clinical scholar. From July 1976 to June 1978, Dr. Thacker served as an Epidemic Intelligence Service (EIS) Officer for CDC, stationed at the Washington, D.C. Health Department. In 1984, he was awarded an M.Sc. in epidemiology from the London School of Hygiene and Tropical Medicine and received certification from the American Board of Preventive Medicine. He currently holds appointments at both Emory University School of Medicine and the Mount Sinai School of Medicine.
Dr. Thacker has published in a broad range of fields in public health, including epidemiology, public health surveillance, meta-analysis, infectious diseases, environmental public health, injury prevention, alcohol abuse, health care delivery, and technology assessment.
Dr. Thacker is a retired Commissioned Officer in the U.S. Public Health Service and is currently holding the grade of Assistant Surgeon General (Rear Admiral, Upper Half).
*** The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.
VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion poker goes up again $
OR-10: Variably protease-sensitive prionopathy is transmissible in bank voles
Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1 Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome, Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna, Italy; 3Case Western Reserve University; Cleveland, OH USA
Background. Variably protease-sensitive prionopathy (VPSPr) is a recently described “sporadic”neurodegenerative disease involving prion protein aggregation, which has clinical similarities with non-Alzheimer dementias, such as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is the electrophoretic pattern of PrPSc after digestion with proteinase K (PK). After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern similar to that described in GSS cases. The clinical and pathological features of VPSPr raised the question of the correct classification of VPSPr among prion diseases or other forms of neurodegenerative disorders. Here we report preliminary data on the transmissibility and pathological features of VPSPr cases in bank voles.
Materials and Methods. Seven VPSPr cases were inoculated in two genetic lines of bank voles, carrying either methionine or isoleucine at codon 109 of the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical diagnosis in voles was confirmed by brain pathological assessment and western blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.
Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission in BvM109. Overall, 3 voles were positive with survival time between 290 and 588 d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form of the typical PrP27–30, which was indistinguishable to that previously observed in BvM109 inoculated with sCJDMM1 cases.
In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until now. Overall, 5 voles were positive with survival time between 281 and 596 d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like PrPSc electrophoretic pattern, characterized by low molecular weight PrPres. These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus and the N-terminus. Second passages are in progress from these first successful transmissions.
Conclusions. Preliminary results from transmission studies in bank voles strongly support the notion that VPSPr is a transmissible prion disease. Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.
The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.