Prion Diseases. CMED 526/EPI 526 - May 6 th , 2009 Robert Harrington, DVM, PhD USDA – Agricultural Research Service UW – Dept. of Comparative Medicine email@example.com. Transmissible Spongiform Encephalopathies~Prion Disease. NORMAL. ABNORMAL. PrP c. PrP d. -helix rich.
CMED 526/EPI 526 - May 6th, 2009
Robert Harrington, DVM, PhD
USDA – Agricultural Research Service
UW – Dept. of Comparative Medicine
Prusiner, et al.
Figure 3: Photomicrographs illustrating increased diameter and density of vacuoles in TME positive IC recipient (top row, a, b, c), as compared to CWD positive IC recipient, (middle row, d, e, f) and absence of lesions in CWD negative IC recipient (bottom, row, g, h, i). Left column = cerebral cortex, middle column = hippocampus, right column = thalamus. All sections stained with hematoxylin and eosin. Bar=100 µm.
Jackson, G S et al. Mol Pathol 2001;54:393-399
vertical and horizontal
in utero, fetal fluids, fetal membranes
Oral (urine, feces, or blood?)
Direct only through bite wounds
No direct transmission
from cow to cow
tissue transplant, HGH, instruments
SOURCE → → → → → → HOST ROUTE
Transmissible Spongiform Encephalopathy as a Zoonotic Disease, Brown, P., et. al. ILSI, March 2003
# Excludes blood transfusion-associated vCJD and pituitary hormone- or dural graft-associated CJD
* UK vCJD deaths, including UK-related nonresident cases, 1995-2003 (Will, RG; personal communication, 2004)
** US CJD deaths, 1995- 2001.
Hilton, 2006. J of Pathology, 208:134
Did the study authors take adequate measures to address the limitations to the study design?What other measures could they have considered?