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The Ecology of Prions
Mark Zabel, Aimee Ortega
Prion Research Center at Colorado State University, Department of Microbiology, Immunology and Pathology,
College of Veterinary Medicine and Biomedical Sciences, Fort Collins, Colorado, USA
SUMMARY ........................................................................................1
INTRODUCTION ..................................................................................1
THE EMERGENCE OF CWD .....................................................................2
ROLE FOR THE ENVIRONMENT IN INDIRECT CWD TRANSMISSION ......................3
POTENTIAL ENVIRONMENTAL PRION RESERVOIRS AND VECTORS ...................... 4
MODELING INDIRECT PRION TRANSMISSION DYNAMICS .................................6
MITIGATING ENVIRONMENTAL PRION CONTAMINATION .................................6
ACKNOWLEDGMENTS ...........................................................................7
REFERENCES ......................................................................................7
AUTHOR BIOS ...................................................................................10
SUMMARY Chronic wasting disease (CWD) affects cervids and is the only known prion
disease readily transmitted among free-ranging wild animal populations in nature. The
increasing spread and prevalence of CWD among cervid populations threaten the sur-
vival of deer and elk herds in North America, and potentially beyond. This review fo-
cuses on prion ecology, specifically that of CWD, and the current understanding of the
role that the environment may play in disease propagation. We recount the discovery of
CWD, discuss the role of the environment in indirect CWD transmission, and consider
potentially relevant environmental reservoirs and vectors. We conclude by discussing
how understanding the environmental persistence of CWD lends insight into transmis-
sion dynamics and potential management and mitigation strategies.
KEYWORDS prions, chronic wasting disease, cervids, soil, water, plants, ecology,
environment, transmission
INTRODUCTION
Transmissible spongiform encephalopathies (TSEs) are a group of diseases caused by
a unique infectious agent, the prion. The prion hypothesis asserts that prions arise
from the misfolding of a normal host protein, the cellular prion protein (PrP
C
), into an
abnormal, pathological isoform resistant to protease degradation (PrP
RES
)(1). Amyloid
deposits of PrP
RES
and spongiform degeneration in the brain characterize TSEs (2).
Clinical signs can vary among TSEs and include wasting, increased salivation, and
general motor impairment. Prions, but not PrP
C
, resist inactivation by ionizing radiation,
formalin, protease and nuclease treatment, and even autoclaving. Numerous TSEs exist
that affect humans and other animals. Chronic wasting disease (CWD) is an animal TSE
that affects cervids, such as elk (Cervus candensis), deer (Odocoileus hemionus), moose
(Alces alces), caribou, and reindeer (Rangifer tarandus), and has become endemic in
both free-ranging and captive herds (3–5). The exact mechanisms of CWD spread
remain unclear, but experimental evidence and mathematical models support a role for
environmental reservoirs and, potentially, vectors in CWD transmission dynamics (6, 7)
(Fig. 1). Population densities and contact frequencies can also influence CWD spread
and transmission (8–10). Water, soil, feces, fomites, and plants may act as environmen-
tal reservoirs (7, 11–14). Continued spread in free-ranging populations, the recent
discovery of CWD in Norway (15), and purported long-term outcomes forecast possible
extinction events. The survival of cervid populations worldwide depends on under-
Published 31 May 2017
Citation Zabel M, Ortega A. 2017. The ecology
of prions. Microbiol Mol Biol Rev 81:e00001-17.
https://doi.org/10.1128/MMBR.00001-17.
Copyright ©2017 American Society for
Microbiology. All Rights Reserved.
Address correspondence to Mark Zabel,
mzabel@colostate.edu.
REVIEW
crossm
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standing the role of the environment in CWD transmission for the development of
effective surveillance, containment, and mitigation strategies.
THE EMERGENCE OF CWD
The discovery of CWD happened incrementally, and over this time, CWD became
endemic in both free-ranging and captive animal herds. A population of captive deer
being held in wildlife facilities in Colorado from 1967 to 1979 were noted to have been
experiencing the same group of clinical signs, including weight loss, torpor, polydipsia,
polyuria, low urine specific gravity, and hypotonia. Histopathological changes were
noted in brain tissue and included spongiform degeneration and vacuolization (3).
There were similarities to other TSEs, both human and animal, but no evidence of CWD
transmission, only some indirect contact between animals at fence lines. Two years
later, the same researchers reported disease phenotypes in Rocky Mountain elk and in
free-ranging cervids as well (16). Amyloid plaques were also noted in the brains of
affected deer (17). Intracranial inoculation of brain homogenates from affected deer
into naive deer and ferrets transmitted CWD after an incubation time of 17 to 24
months (4, 18). Prion amyloids found in the brains of CWD-affected elk and deer
provided evidence of CWD sharing the same etiology and pathology as those of other
TSEs (19, 20).
The origin of CWD is still widely contested. It remains uncertain whether CWD arose
spontaneously as a sporadic incident in one or a few free-ranging or captive deer and
then spread to other cervids across landscapes. No evidence demonstrates CWD being
caused by infected feed or feed products, as occurred in cattle to cause bovine
spongiform encephalopathy (BSE) (21, 22). The scrapie-BSE nexus drives one popular
hypothesis that scrapie crossed the species barrier from sheep to deer when animals
were housed concurrently in Colorado facilities. It may then have spread to and from
free-ranging animals when they came into fence-line contact with captive animals (4).
Most, if not all, CWD cases can be tracked back to movement of infected captive cervids
from the initial epicenter in northern Colorado and southern Wyoming to game farms
FIG 1 CWD prion ecology. Shown is the potential movement of CWD prions in the environment. While
direct transmission likely contributes the most to CWD spread, indirect transmission also occurs via CWD
prion deposition into the environment from urine, feces, and saliva onto and into water, soil, and plants.
Cervids and other animals likely consume prions contained in these reservoirs and become infected.
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throughout North America and South Korea, supporting that hypothesis. While not
linked to CWD emergence in North America, new CWD cases recently discovered in
Norway (15) may be attributed to free-ranging reindeer and moose acquiring the
disease from sympatric scrapie-infected sheep. However, the relatively facile sponta-
neous conversion of cervid PrP
C
to CWD prions in vitro (23) suggests that CWD may
occur spontaneously, like scrapie or sporadic Creutzfeldt-Jakob disease (CJD).
Numerous PRNP gene polymorphisms increase susceptibility or resistance to disease
in deer and elk. The most common mule deer genotypes at codons 95, 96, 132, 138,
and 225 encode glutamine (Q), glycine (G), serine (S), methionine (M), and serine (S),
respectively. Less common polymorphisms include histidine (H) at codon 95, S96,
leucine (L) at codon 132, asparagine (N) at codon 138, and phenylalanine (F) at codon
225. Transgenic mouse experiments convincingly show that the more common geno-
types correlate with increased susceptibility to CWD (24–26). Comparisons between
free-ranging and captive Rocky Mountain elk linked CWD susceptibility to M132
homozygosity (25). Most genotyped CWD-negative deer from Wisconsin expressed
genotypes linked to CWD-positive deer, revealing a huge deer population susceptible
to CWD (24). Evidence that resistant genotypes provide delayed onset or prolonged
incubation periods has been shown, but these genotypes are rarely found in large
populations (27–29). These data alert surveillance and other wildlife management
agencies to be aware of the susceptible populations in their areas and to possibly
mitigate continued spread based on this information.
ROLE FOR THE ENVIRONMENT IN INDIRECT CWD TRANSMISSION
In the 1940s, shepherds in northern Iceland culled their entire sheep population
in an effort to eradicate Maedi, an ovine lung disease rampant in their flocks. The
area in which the culling took place overlapped areas where evidence supported
the presence of scrapie, the prion disease of sheep. Healthy sheep from an area with
no evidence of scrapie were introduced into this area. After 3 years, the new animals
became sick with scrapie (30–32). In 1978, Iceland again tried to eradicate scrapie
by imposing strict implementations, including culling positive and at-risk animals,
disinfecting or destroying buildings that housed infected animals, banning trans-
location of animals and equipment from positive farms, restocking farms after at
least two dormant years, and continued surveillance. After 16 years, some of the
reintroduced flocks developed clinical scrapie (30). Because these flocks had been
scrapie-free through several generations, the environmental persistence of scrapie
prions on these farms likely contributed to the emergence of new scrapie cases in
these sheep.
Similar environmental persistence has been noted with CWD. The Foothills Wildlife
Research Facility (FWRF) in Fort Collins, CO, where CWD was originally detected, underwent
a similar cleansing and culling in order to eradicate CWD and to establish new,
CWD-free herds. Approximately 2 years after reintroduction of elk herds to the FWRF,
animals began showing clinical signs of illness. These decontamination failures impli-
cated environmental reservoirs in the reemergence of CWD in these herds, all of whose
members were acquired from Rocky Mountain National Park as calves, born to wild
free-ranging dams, when they were less than 1 week old (33). While the reoccurrence
of infection may have been from environmental persistence and indirect transmission
of cervid prions, vertical transmission from positive mothers infecting their calves also
may have occurred. As CWD progressed, animals may have begun shedding prions,
leading to both a direct contact source between elk and an indirect source via
accumulation in paddocks. An experimental demonstration of indirect environmental
reservoir transmission was shown in 2004, when uninfected mule deer were housed in
paddocks containing either infected deer or a positive deer carcass decomposed 20
months prior or in an empty paddock containing excreta from positive deer housed 26
months prior. Uninfected deer became CWD positive in all three scenarios (34). CWD
transmission increases during winter, possibly due to density-dependent transmission.
Deer herds stay together over winter, which may increase the chance of both direct
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transmission and contacting accumulated positive environmental material. Indeed, the
prevalence of CWD has been shown to be much higher in defined winter ranges, which
may be due to an accumulation of PrP-positive material in these areas (35).
Bedding and water transferred from indoor rooms housing CWD-positive deer
transmitted CWD to negative deer in prion-naive rooms in only 15 months. Tonsil
biopsy confirmed the presence of PrP
CWD
in one of two animals (13). Both animals
eventually contracted CWD solely through environmental exposure. Given the over-
whelming evidence that prions resist degradation, persist in the environment for years
(30), and can be shed in excreta of clinical as well as asymptomatic animals (12, 36–39),
CWD prions likely accumulate in the environment. Estimation of prion titers by mouse
bioassay of CWD prions intracerebrally inoculated into susceptible animals indicates
that a single experimentally inoculated deer can defecate 10.9 log 50% lethal dose
(LD
50
) units of CWD prions over a 10-month period, a typical duration of CWD (39). The
same deer can also urinate up to 6 log LD
50
units of prions into the environment over
this time. Naturally infected deer defecate an estimated 1,000 LD
50
units of CWD prions
daily (12). While these doses are relatively low, repeated frequent exposure, either
direct or indirect, increases the likelihood of contracting CWD (7, 40).
POTENTIAL ENVIRONMENTAL PRION RESERVOIRS AND VECTORS
Researchers are currently investigating at least three potential environmental res-
ervoirs for prions—soil, water, and plants. These proposed reservoirs most likely
accumulate prions deposited from excreta and decaying carcasses. Other fomites in the
environment, such as salt licks, wallows, fences, bedding sites, and even buildings, may
also contribute to prion deposition in the environment (13, 30, 41, 42).
Deer and elk ingest small but appreciable amounts of soil (⬍2% soil consumption
in the diet) (7, 43). They often ingest soil inadvertently while feeding, but they may also
intentionally eat soil to obtain micronutrients essential to their metabolism. These
considerations led researchers to begin looking for prions in soil and to determine
whether PrP
C
binds soil and/or its constituents and if the prion infectivity and/or
conformation changes in a soil environment. One study looked at the potential ability
of PrP
C
to misfold into the pathological prion structure when bound to a mineral-phase
soil component known as montmorillonite (MTE) (44). While PrP-MTE complexes were
formed and some
␣
-helical-to-

-sheet-like structural changes occurred, these structural
transformations were distinct from the pH-induced conformational changes that occur
during prion formation and did not produce infectious prions. Similar work demon-
strated that prions could also adsorb to MTE, microparticles of quartz, kaolinite (another
mineral-phase soil component), and a variety of whole soils (45). MTE bound prions so
tightly that 10% sodium dodecyl sulfate was required for desorption and resulted in
N-terminal truncation of PrP
RES
. Prions present in a complex matrix of infected brain
homogenate adsorbed to MTE much more slowly, which likely mimics environmental
contamination (46). Experimental evidence shows that unbound prions degrade over
time, while soil-bound prions remain at stable or increasing levels (47, 48), suggesting
that prions remain stable in the environment when bound to soil or clay components
and potentially become more infectious. Prions remained infectious when bound to
MTE and inoculated intracranially into rodents (49). MTE was recently shown to increase
the environmental stability and bioavailability of prions bound to it (7). However, when
prions were subjected to simulated weather conditions, such as heating, wetting, and
drying, MTE actually potentiated prion degradation (50). Microbial communities in soil,
compost, and lichens also demonstrate significant reductions of prion titers (51–53).
Thus, natural and cultivated microbial communities may mitigate some, but not all,
environmental prion contamination.
Prions that do survive environmental insult maintain or even augment prion trans-
mission. Prion infectivity and oral transmission increased when PrP was bound to soil
(54). Intranasal inoculations of deer with prions bound to MTE dust particles resulted in
efficient transmission of CWD (55). Soil-bound prions resist rumen digestion, and MTE
enhances the bioavailability and retention of prions bound to it (56). This high affinity
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of MTE for prions potentially may be exploited as a therapeutic or decontaminant to
remove PrP from complex solutions.
Nichols et al. found PrP
RES
in water collected from an area in Colorado where CWD
is endemic and from raw water samples collected in a nearby water treatment facility
(11). BSE prions survived in raw sewage, with little or no reduction in infectivity (57), and
organic matter present in water partially prevented degradation of PrP
RES
and loss of
infectivity (58, 59). Fomites from infected deer, including water, transmitted CWD prions
to uninfected deer with no direct contact with infected cohorts (13).
Detection of prions in soil, water, excreta, and decaying carcasses on the landscape
raises legitimate concern about whether plants, the main food source of deer and elk,
can act as prion vectors by active uptake or passive contamination. Plants take up
protein, as a nitrogen source, and other nutrients in their roots, stems, and aerial tissues
(60–62). Endophytic bacteria and bacterial communities that fix nitrogen and fight
plant diseases have been described (61, 63, 64). Plants may conceivably take up prions
from soil or water into their root systems or aerial tissues or become surface contam-
inated through saliva, urine, feces, and/or decaying CWD-infected carcasses. An at-
tempt was made to assess the potential of wheat grass grown in agar medium to take
up prions from water (65). Both roots and lower stems were examined for PrP
RES
by
using commercially available enzyme-linked immunosorbent assays for PrP
RES
and an
ultrasensitive prion detection assay, i.e., protein misfolding cyclic amplification (PMCA).
The researchers reported finding PrP
RES
inside roots but not stems, in addition to PrP
RES
on stem and root surfaces that was rinsed away with water. PMCA experiments were
inconclusive due to nonspecific amplification in control unexposed plant homogenates.
Prion uptake was assessed for only one 24-h time point, and significant contamination
issues were reported. Another group successfully used PMCA to detect prions taken
into roots, stems, and leaves by wheat grass plants (Triticum aestivum L.) grown with
high concentrations of prions spiked into soil (14). Since copious data show that soil
binds prions extremely tightly, the mechanism by which prions move from soil to plants
remains unclear. Perhaps the experimental conditions used soil saturated with prions
and facilitated plant uptake of free prions. If so, these results may not be ecologically
relevant, since one expects very low levels of prion contamination, except perhaps in
areas just under a decaying infected carcass. More relevant experimental contamina-
tion of plants by spraying of infected brain homogenate onto wheat (Triticum aestivum
L.) leaves resulted in detection of PrP
RES
at a stable level for 49 days. Different plant
tissues were also exposed to urine and feces from both CWD-positive animals and
scrapie-infected hamsters, and the results again showed prions bound to the plant
tissues after rinsing and drying.
Decaying carcasses of any kind affect the ecosystem around them, often leading
to higher concentrations of nitrogen and a difference in plant species in the area
that may be present for years after the initial decomposition. As a carcass decays,
the body fluids released destroy the plants underneath and in the surrounding area,
creating a zone of disturbance which, after time, becomes zones of fertility due to
nutrients and limited competition from other species (66). Since CWD prions have
been shown to persist in the environment, it is postulated that a decaying CWD-
positive carcass can saturate the environment with prions, which can then be taken
up into plants as growth of new flora occurs. Prions were detected in roots, stems,
and leaves of wheat plants (Hordeum vulgar) grown in soil experimentally contam-
inated with prions (14). Cervids readily eat both wheat and barley grasses in the
spring: around 4 to 64% of the mule deer diet is composed of grasses, while the
remainder comes from shrubs and trees (67).
Reservoir or vector animals transmit many emerging infectious diseases that affect
wildlife populations. No reservoir animals have been found for CWD, although several
vector animals, including predators and scavengers, may aid in dissemination of CWD
prions across the landscape. Coyotes (68), cougars (69), and even crows (70) have been
investigated as potential CWD reservoirs and/or vectors. Experimentally inoculated
coyotes and crows both shed infectious prions in their feces. Both mammalian and
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avian scavengers travel scores of kilometers per day and likely contribute to prion
dissemination across their habitats and prion accumulation across landscapes. While
cougars prey more successfully on CWD-affected cervids than on unaffected cervids, no
evidence exists that cougars have contracted feline spongiform encephalopathy as a result.
Thus, if they contribute to prion dissemination, they likely do so as vectors, not reservoirs.
Even if reservoir species do exist, they likely replicate prions as a new strain that
likely exhibits altered host ranges and introduces new species barriers to cervids
and other mammals that contact them. But Bian et al. recently demonstrated
nonadapted prion amplification (NAPA) experimentally in vitro and in vivo (71), so
host range restriction by reservoir animals may not be absolute. If NAPA occurs in
nature, prion dissemination may aid environmental prion reservoirs to perpetuate
CWD via indirect transmission. In the absence of CWD reservoir animals, transloca-
tion of CWD-infected cervids often facilitates emergence, because it can bring
susceptible naive animals in contact with infected ones and their contaminated
environments (72), providing proximity to CWD prion reservoirs for both direct and
indirect transmission.
MODELING INDIRECT PRION TRANSMISSION DYNAMICS
Mathematical models of CWD prevalence and dynamics support the hypothesis that
direct transmission certainly accounts for most transmission events, with both popu-
lation density and contact frequency contributing to CWD spread (9, 73). However,
modeling of only direct transmission failed to account for data showing high and
increasing prevalences in areas of endemicity (74, 75). Modeling of exposure risks of
sheep flocks to scrapie identified buildings and pastures as likely sources of indirect
scrapie transmission (76). Models of CWD transmission that include both direct and
indirect parameters more closely match the available data on current epidemics seen
in Colorado, Wyoming, and Wisconsin (6, 10). Miller et al. compared seven different
CWD transmission models and found that those including indirect transmission param-
eters matched existing data four times more accurately than those modeling only direct
transmission (75). Including landscape effects derived from GPS data in areas of Alberta,
Canada, where CWD is endemic increased the precision of models using density
parameters (8). Bayesian models assuming a long prion half-life implicate a significant
role for indirect CWD prion exposure in CWD transmission dynamics due to accumu-
lating prions in the environment (74, 77). They also model a slowly progressing disease
that predicts a potential nonfatal carrier state that may ameliorate population decline
initially but accelerate transmission as environmental contamination mounts, a conclu-
sion corroborated by another model considering prolonged environmental prion per-
sistence (78). Repeated sampling of the same mule deer populations in Colorado
informed another Bayesian hierarchical model that predicted a steady population
decline that could be slowed by hunter harvest, vehicular deaths, and predation (6).
Few data or models predict sex-dependent transmission, although one model pre-
dicted that sex-specific differences fit frequency-dependent transmission models better
(9). However, the authors included no indirect transmission parameter in their
model, which may not accurately fit existing data dependent on the level of
environmental accumulation. CWD prevalence continues to increase from Wyoming
to Wisconsin to Arkansas, with these areas of endemicity reporting estimates
ranging from 15 to 50% for free-ranging populations (47). With CWD spreading
unabated, prion loads accumulating and persisting on landscapes, and the preva-
lence continuing to increase, both mathematical models and epidemiological data
suggest that a tipping point may be reached, potentially resulting in herd decima-
tion and population decline, especially in the presence of environmental reservoirs
that retain prions for extended periods.
MITIGATING ENVIRONMENTAL PRION CONTAMINATION
Continued spread of CWD is clearly a multifaceted event. Prion persistence, indirect
transmission, genetics, population density, contact frequency, management strategies,
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and other unrealized factors all may affect CWD ecology. Emerging data support a
possibly significant role of soil, water, feces, and plants as prion reservoirs contributing
to environmental contamination and indirect CWD transmission. CWD has now been
found in cervids in 22 U.S. states, 2 Canadian provinces, South Korea, and Norway (5,
15). As CWD continues to unabatedly establish endemicity wherever it appears, elim-
inating or reducing environmental prion loads across landscapes represents a critical
but enormous challenge.
Researchers have demonstrated that composting, incineration, and enzyme
treatments may help to degrade environmental PrP
RES
(53,79,80). These studies
have focused mainly on specified risk material (SRM) generated from abattoirs and
commercial meat processing plants. Brown et al. detected residual prion infectivity
even after incineration at 600°C, although the initial prion titer was over 10
9
LD
50
units/g of tissue (80), which is well beyond realistic environmental prion titers.
Composting reduces prion titers in SRM by a much more modest 1 to 2 log, with
cultivation of a proteolytic microbiome eliminating another order of magnitude of
infectivity (53). Robust prion oxidation by ozone treatment also reduces prion
infectivity in SRM and contaminated wastewater, by several orders of magnitude
(81,82). These procedures may be effective for reducing the likelihood of contam-
inating environments proximal to industrial farming enterprises but are impractical
or simply cannot be applied to massive areas contaminated by CWD prions depos-
ited by infected cervids across three continents. Although sources of CWD prions
that contaminate endemic environments contain low levels of prions, continuous
prion deposition and sustained prion persistence in environmental reservoirs pose
significant challenges for bioremediation. Infected free-ranging animals continu-
ously shedding prions in the environment and large host ranges complicate
environmental decontamination strategies, especially if free-ranging infected ani-
mals cannot be removed, cordoned, or quarantined and contaminated landscapes
protected from infected cervids returning to those habitats. Recontamination will
likely occur and population decline will likely result if mitigation strategies fail. More
sampling and surveillance need to be undertaken to understand the extent of
environmental contamination in different areas of endemicity, and new mitigation
strategies should be explored.
Controlled burning of landscapes in North America helps to mitigate fire danger in
drought-stricken areas, in some of which CWD is endemic. Burning of plants, feces, and
topsoil in these areas may reduce the low-level prion infectivity present in these areas.
While the burn temperature and duration are certainly much lower than those attained in
the experiments for which Brown et al. reported residual prion infectivity, naturally CWD-
contaminated areas certainly contain many orders of magnitude less prion infectivity than
prion-infected SRM. Prescribed burning may sufficiently lower prion titers on landscapes to
at least impede the indirect transmission of CWD. Combined with directed hunter harvests,
systematic culling, and targeted implementation of CWD vaccines (83,84), we may be able
to stem the slow but steady spread of CWD across the landscape.
ACKNOWLEDGMENTS
We thank Jan Leach, Jeff Wilusz, and Candace Mathiason for critical readings of this
review.
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Ecology of Prions Microbiology and Molecular Biology Reviews
September 2017 Volume 81 Issue 3 e00001-17 mmbr.asm.org 9
on May 31, 2017 by guesthttp://mmbr.asm.org/Downloaded from
Mark Zabel earned his Ph.D. in experimental
pathology in the lab of John H. Weis at the
University of Utah School of Medicine, with
training in prion biology, biochemistry, and
immunology from Adriano Aguzzi at the In-
stitüt for Neuropathology, Universitätspital
Zürich, Zurich, Switzerland. He is currently
Associate Director of the Prion Research
Center and Professor in the Department of
Microbiology, Immunology and Pathology,
College of Veterinary Medicine and Biomed-
ical Sciences, Colorado State University. Dr. Zabel collaborates with
researchers at the USDA National Wildlife Research Center, the National
Park Service, Colorado Parks and Wildlife, and Rocky Mountain National
Park. These collaborators seek to understand CWD prevalence in cervids
and prion movement in the environment, with the ultimate goal of
developing vaccines, therapeutics, and CWD management and mitiga-
tion strategies to stem the tide of CWD spread across landscapes. Dr.
Zabel enjoys the opportunities to work outside to achieve these goals.
Aimee Ortega earned her M.S. in microbiol-
ogy in the Zabel laboratory at the Prion
Research Center at Colorado State Univer-
sity, Department of Microbiology, Immunol-
ogy and Pathology, College of Veterinary
Medicine and Biomedical Sciences. She drove
the project to evaluate the role of plants as a
CWD prion reservoir in the environment and
as vectors for indirect CWD transmission. She
is currently a clinical research scientist at the
Veterans Administration Medical Center in
Denver, CO. Aimee’s thesis committee encouraged her to write this
review article as an extension of the introduction to her thesis. Aimee
is an accomplished researcher, avid backpacker, and science advocate.
Zabel and Ortega Microbiology and Molecular Biology Reviews
September 2017 Volume 81 Issue 3 e00001-17 mmbr.asm.org 10
on May 31, 2017 by guesthttp://mmbr.asm.org/Downloaded from
