Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions

[Emily]

[h=4]Grass Plants Bind, Retain, Uptake, and Transport Infectious Prions[/h] Pritzkow, Sandra et al.
Cell Reports , Volume 11 , Issue 8 , 1168 - 1175 [h=2]Highlights[/h]

• ?Grass plants bind prions from contaminated brain and excreta
• ?Prions from different strains and species remain bound to living plants
• ?Hamsters fed with prion-contaminated plant samples develop prion disease
• ?Stems and leaves from grass plants grown in infected soil contain prions

[h=2]Summary[/h] Prions are the protein-based infectious agents responsible for prion diseases. Environmental prion contamination has been implicated in disease transmission. Here, we analyzed the binding and retention of infectious prion protein (PrP[SUP]Sc[/SUP]) to plants. Small quantities of PrP[SUP]Sc[/SUP] contained in diluted brain homogenate or in excretory materials (urine and feces) can bind to wheat grass roots and leaves. Wild-type hamsters were efficiently infected by ingestion of prion-contaminated plants. The prion-plant interaction occurs with prions from diverse origins, including chronic wasting disease. Furthermore, leaves contaminated by spraying with a prion-containing preparation retained PrP[SUP]Sc[/SUP] for several weeks in the living plant. Finally, plants can uptake prions from contaminated soil and transport them to aerial parts of the plant (stem and leaves). These findings demonstrate that plants can efficiently bind infectious prions and act as carriers of infectivity, suggesting a possible role of environmental prion contamination in the horizontal transmission of the disease.

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

Received: October 31, 2014; Received in revised form: February 4, 2015; Accepted: April 15, 2015; Published Online: May 14, 2015
? 2015 The Authors. Published by Elsevier Inc.

http://www.cell.com/cell-reports/abstract/S2211-1247(15)00437-4

Full text

 

[Amish Country]

Does this mean that the pirons are permanently in the effected vegetation and can potential be transmitted to what ever animal eats it or the disease is only transmittable via this vector for a few weeks after the initial contamination? If it is the later would feeding slightly aged dried hay or grain prevent potential transmission of the disease? After the vegetation has died and decomposed are the prions then taken back up into plants fertilized by the compost?

 

[Emily]

Does this mean that the pirons are permanently in the effected vegetation and can potential be transmitted to what ever animal eats it or the disease is only transmittable via this vector for a few weeks after the initial contamination? If it is the later would feeding slightly aged dried hay or grain prevent potential transmission of the disease? After the vegetation has died and decomposed are the prions then taken back up into plants fertilized by the compost?

Those are good questions, Amish. It would be great if prions taken into grasses did inactivate after a period of time. Right now the research looks preliminary.

?This research was done in experimental conditions in the lab,? Soto said of the next step. ?We?re moving the research into environmental contamination now.?

https://www.uth.edu/media/story.htm?id=7ab3d80c-46f7-4ed1-b711-3540bd1c688d

CWD is very different than other TSE's in some aspects. 100% of deer are susceptible. In kuru, I think only 10-20% of the Fore population was susceptible. The disease would have eventually burned out even if cultural practices had not changed. I don't think the picture is so optimistic for CWD, especially with the shedding in urine and feces.

The timeline on CWD is interesting:
http://www.cwd-info.org/index.php/f...t+(WDIN+-+New+Chronic+Wasting+Disease+Content

So found in CO research facilities in 1967 but never in the wild until 1981 - 14 years later! It would have been hard to miss the symptoms:

Journal of Wildlife Diseases 16(1):89-98. 1980
[h=5]CHRONIC WASTING DISEASE OF CAPTIVE MULE DEER: A SPONGIFORM ENCEPHALOPATHY[SUP]1[/SUP][/h]
E. S. WILLIAMS and S. YOUNG
Wild Animal Disease Center and Department of Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, Colorado 80523, USA



[SUP]1[/SUP]This study was supported in part by N.I.H. (BRSG) Grant 5S07-RR-05458-17
In the past 12 years (1967?79) a syndrome we identify as chronic wasting disease has been observed in 53 mule deer (Odocoileus hemionus hemionus) and one black-tailed deer (Odocoileus hemionus columbianus) held in captivity in several wildlife facilities in Colorado and more recently in Wyoming. Clinical signs were seen in adult deer and included behavioral alterations, progressive weight loss and death in 2 weeks to 8 months. Gross necropsy findings included emaciation and excess rumen fluid admixed with sand and gravel. Consistent histopathologic change was limited to the central nervous system and characterized by widespread spongiform transformation of the neuropil, single or multiple intracytoplasmic vacuoles in neuronal perikaryons and intense astrocytic hypertrophy and hyperplasia. Presented is a clinical characterization of chronic wasting disease and pathologic evidence supporting the conclusion that the disease is a specific spontaneously occurring form of spongiform encephalopathy.


Received: September 11, 1979
...

Clinical signs of CWD occurred only in
mule deer maintained in captivity for a
period of 2.5 to 4 years, whether raised
from infancy by hand or captured in the
wild as young adults. The disease
affected males, females and castrates.
Listlessness, progressive weight loss and
depression with insidious onset and
protracted course occurred over 2 weeks
to 8 months, leading to emaciation (Fig.
1) and death. Onset occurred during all
seasons. The majority of affected deer
developed signs of polydipsia, polyuria,
excessive salivation, grinding of the
teeth, flaccid hypotonia of facial
muscles, lowering of the head, drooping
of the ears and terminal anorexia. In
some affected animals esophageal
hypotonia and dilatation, difficulty in
swallowing, regurgitation of rumenal
fluid and ingesta, and depraved appetite
occurred. Behavioral changes included
episodes of apparent lack of awareness.
Affected deer often stood for several
minutes with lowered head and a fixed
stare, and then reverted to a more normal
state of alertness. Decreased interactions
with unaffected deer in the group, occasional
abnormal response to restraint
and hyperexcitability were noted,
Although behavioral changes were a
consistent feature of CWD, specific motor
or sensory neurologic signs were not
identified. Equivocal visual deficits occasionally
were suspected. In many instances,
the disease was interrupted or
terminated by secondary complications,
notably pneumonia, or by euthanasia...

However CWD emerged, let's hope it doesn't happen in other species.

 

[Emily]

[h=1]Much still unknown about CWD?s effect on humans[/h] Patrick Durkin, For Gannett Wisconsin Media 2:04 p.m. CDT July 24, 2015

... David Clausen, a retired veterinarian who served 7? years on the seven-citizen DNR Board, including four years as its chair, notes that the DNR tests only one-fifth as many deer as it did in the early 2000s. In fact, in 2014 it tested 80 percent fewer deer than in 2002 and yet found 60 percent more CWD cases.
Clausen said he?s alarmed by the increase in ?positive deer carcasses? likely entering people?s kitchens from Wisconsin?s worst CWD region, which includes Dane, Iowa, Sauk, Rock, Green, Columbia, Lafayette, Richland and Walworth counties....
... Clausen concedes there is no evidence humans have contracted CWD from eating infected venison, and that the odds of it transmitting to humans probably remain small. However, ?the odds have never been zero.? Clausen notes that a 2005 study that reported a ?substantial? species barrier from elk and deer to humans was recently revised after new findings prompted its authors to re-examine tissues from the original study.
?Upon further review, their study and another recent study (which found 2 in 20 ?humanized? transgenic mice with clinical prion infections) pretty much blow the original study out of the water,? Clausen said. ...
... Clausen said other research makes him wonder if venison consumption should be our primary concern. Researchers at the University of Texas Houston and Colorado State University found that wheat grass surfaces contaminated by urine, brain and feces were not easily washed clean. Further, Chris Johnson at the National Wildlife Heath Center in Madison found that alfalfa, barley, corn and tomatoes could take up prions from the soil. And hamsters fed prion-contaminated plant samples in the UTH and CSU study developed prion disease.
Clausen thinks the possibilities of plant-based CWD infections could eventually threaten agriculture in Wisconsin and the United States...

http://www.greenbaypressgazette.com...ch-still-unknown-cwds-effect-humans/30629083/