Models Qingzhong Kong, Ph.D., Assistant Professor, Pathology, Case Western Reserve
University

 

Bovine Amyloid Spongiform Encephalopathy (BASE) is an atypical BSE strain
discovered recently in Italy, and similar or different atypical BSE cases
were also reported in other countries. The infectivity and phenotypes of
these atypical BSE strains in humans are unknown. In collaboration with
Pierluigi Gambetti, as well as Maria Caramelli and her co-workers, we have
inoculated transgenic mice expressing human prion protein with brain
homogenates from BASE or BSE infected cattle. Our data shows that about half
of the BASE-inoculated mice became infected with an average incubation time
of about 19 months; in contrast, none of the BSE-inoculated mice appear to
be infected after more than 2 years.

 

***These results indicate that BASE is transmissible to humans and suggest that BASE is more virulent than
classical BSE in humans.***

 

6:30 Close of Day One

 

 

 

 

SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM
1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...

 

 

 

 

There is a growing number of human CJD cases, and they were presented last
week in San Francisco by Luigi Gambatti(?) from his CJD surveillance
collection.

 

He estimates that it may be up to 14 or 15 persons which display selectively
SPRPSC and practically no detected RPRPSC proteins.

 

 

 

[Docket No. FSIS-2006-0011] FSIS Harvard Risk Assessment of Bovine
Spongiform Encephalopathy (BSE)

 

 

[Docket No. 03-025IFA] FSIS Prohibition of the Use of Specified Risk
Materials for Human Food and Requirement for the Disposition of
Non-Ambulatory Disabled Cattle

 

 

 

THE SEVEN SCIENTIST REPORT ***

 

 

Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION]

 

 

Docket Management Docket: 02N-0273 - Substances Prohibited From Use in

 

Animal Food or Feed; Animal Proteins Prohibited in Ruminant Feed

 

Comment Number: EC -10

 

Accepted - Volume 2

 

 

PART 2

 

 

THE USDA JUNE 2004 ENHANCED BSE SURVEILLANCE PROGRAM WAS TERRIBLY FLAWED ;

 

CDC DR. PAUL BROWN TSE EXPERT COMMENTS 2006

 

The U.S. Department of Agriculture was quick to assure the public earlier
this week that the third case of mad cow disease did not pose a risk to
them, but what federal officials have not acknowledged is that this latest
case indicates the deadly disease has been circulating in U.S. herds for at
least a decade.

 

The second case, which was detected last year in a Texas cow and which USDA
officials were reluctant to verify, was approximately 12 years old.

 

These two cases (the latest was detected in an Alabama cow) present a
picture of the disease having been here for 10 years or so, since it is
thought that cows usually contract the disease from contaminated feed they
consume as calves. The concern is that humans can contract a fatal,
incurable, brain-wasting illness from consuming beef products contaminated
with the mad cow pathogen.

 

"The fact the Texas cow showed up fairly clearly implied the existence of
other undetected cases," Dr. Paul Brown, former medical director of the
National Institutes of Health's Laboratory for Central Nervous System
Studies and an expert on mad cow-like diseases, told United Press
International. "The question was, 'How many?' and we still can't answer
that."

 

Brown, who is preparing a scientific paper based on the latest two mad cow
cases to estimate the maximum number of infected cows that occurred in the
United States, said he has "absolutely no confidence in USDA tests before
one year ago" because of the agency's reluctance to retest the Texas cow
that initially tested positive.

 

USDA officials finally retested the cow and confirmed it was infected seven
months later, but only at the insistence of the agency's inspector general.

 

"Everything they did on the Texas cow makes everything USDA did before 2005
suspect," Brown said. ...snip...end

 

 

CDC - Bovine Spongiform Encephalopathy and Variant Creutzfeldt ...
Dr. Paul Brown is Senior Research Scientist in the Laboratory of Central
Nervous System ... Address for correspondence: Paul Brown, Building 36, Room
4A-05, ...

 

 

PAUL BROWN COMMENT TO ME ON THIS ISSUE

 

Tuesday, September 12, 2006 11:10 AM

 

"Actually, Terry, I have been critical of the USDA handling of the mad cow
issue for some years, and with Linda Detwiler and others sent lengthy
detailed critiques and recommendations to both the USDA and the Canadian
Food Agency."

 

OR, what the Honorable Phyllis Fong of the OIG found ;

 

Audit Report

 

Animal and Plant Health Inspection Service

 

Bovine Spongiform Encephalopathy (BSE) Surveillance Program – Phase II

 

and

 

Food Safety and Inspection Service

 

Controls Over BSE Sampling, Specified Risk Materials, and Advanced Meat
Recovery Products - Phase III

 

Report No. 50601-10-KC January 2006

 

Finding 2 Inherent Challenges in Identifying and Testing High-Risk Cattle
Still Remain

 

 

 

 

 

 

CJD WATCH

 

 

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

 

Singeltary, Sr et al. JAMA.2001; 285: 733-734.

 

http://jama.ama-assn.org/http://www.neurology.org/cgi/eletters/60/2/176#535

 

BRITISH MEDICAL JOURNAL

 

BMJ

 

http://www.bmj.com/cgi/eletters/319/7220/1312/b#EL2

 

BMJ

 

http://www.bmj.com/cgi/eletters/320/7226/8/b#EL1

 

JOURNAL OF NEUROLOGY

 

MARCH 26, 2003

 

RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob

 

disease in the United States

 

Email Terry S. Singeltary:

 

flounder@wt.net

 

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to

 

comment on the CDC's attempts to monitor the occurrence of emerging

 

forms of CJD. Asante, Collinge et al [1] have reported that BSE

 

transmission to the 129-methionine genotype can lead to an alternate

 

phenotype that is indistinguishable from type 2 PrPSc, the commonest

 

sporadic CJD. However, CJD and all human TSEs are not reportable

 

nationally. CJD and all human TSEs must be made reportable in every

 

state and internationally. I hope that the CDC does not continue to

 

expect us to still believe that the 85%+ of all CJD cases which are

 

sporadic are all spontaneous, without route/source. We have many TSEs in

 

the USA in both animal and man. CWD in deer/elk is spreading rapidly and

 

CWD does transmit to mink, ferret, cattle, and squirrel monkey by

 

intracerebral inoculation. With the known incubation periods in other

 

TSEs, oral transmission studies of CWD may take much longer. Every

 

victim/family of CJD/TSEs should be asked about route and source of this

 

agent. To prolong this will only spread the agent and needlessly expose

 

others. In light of the findings of Asante and Collinge et al, there

 

should be drastic measures to safeguard the medical and surgical arena

 

from sporadic CJDs and all human TSEs. I only ponder how many sporadic

 

CJDs in the USA are type 2 PrPSc?

 

http://www.neurology.org/cgi/eletters/60/2/176#535

 

i did not post this to scare anyone, i am a meateater, but these are the facts, i thought you should know this. ...

 

thank you,
kind regards,
terry

 

 

From: TSS ()
Subject: CWD TWO NEW CASES NEAR WHITE SANDS MISSLE RANGE NEW MEXICO
Date: June 27, 2005 at 4:43 pm PST

 

 

Subject: CWD 3 NEW CASES SOUTHERN NEW MEXICO
Date: July 10, 2006 at 8:51 am PST
New Mexico Department of Game and Fish
Media contact: Dan Williams, (505) 476-8004
Public contact: (505) 476-8000
dan.williams@state.nm.us

 

FOR IMMEDIATE RELEASE, JULY 7, 2006:

 

 

Date:         Thu, 28 Dec 2006 12:03:19 -0600
Reply-To:     Sustainable Agriculture Network Discussion Group

 

Sender:       Sustainable Agriculture Network Discussion Group

 

From:         "Terry S. Singeltary Sr."
Subject:      Fw: CWD in New Mexico 35 MILES FROM TEXAS BORDER and low
testing
              sampling figures -- what gives TAHC ???

 

 

 

 

 

 

Research Project: Transmission, Differentiation, and Pathobiology of
Transmissible Spongiform Encephalopathies
Location: Virus and Prion Diseases of Livestock

 

Title: Experimental Second Passage of Chronic Wasting Disease (Cwd-Mule
Deer) Agent to Cattle

 

 

 

 

 

 

Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518

 

Subject: Transmission of TSEs through ectoparasites i.e. P. tenuis and CWD
Date: May 3, 2007 at 9:05 am PST

 

CONFIDENTIAL
SEAC 97/2
Annex 2
UNITED KINGDOM ACCREDITATION SERVICE (UKAS)
ASSESSMENT REPORT

 

Other organisms

 

Transmission of TSEs through ectoparasites has been postulated by Lupi5.
Post et al6
fed larvae of meat eating and myiasis causing flies with brain material from
scrapieinfected
hamsters. Two days after eating infected material, the larvae showed high
amounts of PrPSc by Western blot. In further studies, the inner organs of
larvae, which
had been fed with scrapie brain, were extracted and fed to hamsters. Six out
of eight
hamsters developed scrapie. Two out of four hamsters fed on scrapie infected
pupae
subsequently developed scrapie.

 

 

I AGAIN raise the possibility of that damn brain eating worm in elk and CWD
transmission via elk, deer, and other critters eating that worm. ...tss

 

Immunodiagnosis of experimental Parelaphostrongylus tenuis infection in elk
Oladele Ogunremi, Murray Lankester, and Alvin Gajadhar
Centre for Animal Parasitology, Canadian Food Inspection Agency, 116
Veterinary Road, Saskatoon, Saskatchewan S7N 2R3 (Ogunremi, Gajadhar);
Department of Biology, Lakehead University, 955 Oliver Road, Thunder Bay,
Ontario P7B 5E1 (Lankester).

 

Elk infected with the meningeal worm, Parelaphostrongylus tenuis
(Protostrongylidae), do not consistently excrete larvae in feces, making the
current method of diagnosing live animals using the Baermann fecal technique
unreliable. Serological diagnosis could prove more useful in diagnosing
field-infected animals but depends on the identification and availability of
good quality antigen. To mimic field infections, 2 elk were inoculated with
6 infective L3 larvae of P. tenuis, and another 2 with 20 L3 larvae. Fecal
samples were examined for nematode larvae using the Baermann technique and
serum samples taken were tested for anti-P. tenuis antibody with ELISAs by
using the excretory-secretory (ES) products of L3, and sonicated adult worms
as antigens. One animal passed first-stage larvae in its feces 202 days
postinoculation, but passed none thereafter. The remaining 3 inoculated
animals did not pass larvae. In contrast to parasite detection, antibodies
against larval ES products were detected in all animals starting from 14 to
28 days postinoculation and persisted until the termination of the
experiment on day 243 in 2 animals that harbored adult worms. Antibodies
against somatic antigens of the adult worm were not detected until day 56
but also persisted until the end of the experiment in the animals with adult
worms. In 2 elk that had no adult worms at necropsy, anti-ES antibodies were
detected transiently in both, while anti-adult worm antibodies were present
transiently in one. These findings confirm the superiority of P. tenuis
larval ES products over somatic adult worm antigens as serodiagnostic
antigens, as previously observed in studies of infected white-tailed deer,
and extend the application of the newly developed ELISA test in diagnosing
and monitoring cervids experimentally infected with P. tenuis.

 

 

Subject: TSE & insects as a vector of potential transmission
Date: October 26, 2006 at 12:50 pm PST

 

i try to keep an open mind about any other routes and sources that we may be
overlooking. i mean, there is enough TSE protein in circulation now VIA the
FDA, just in 2006 alone, and the oral route has been proven with BSE, and
the non-forced oral consumption of scrapie to primate, as to not worry about
a natural route of a few worms that have maybe been feasting on a deer
that's brain is infected with CWD, then excreted out, and then passed on to
another worm hungry deer looking for that feast. i suppose maybe just
another potential route and source for a TSE, and possibly even a 'double
dose' so to speak from not only the worm in the feces (maybe triple with
feces), but the soil as well (see soil and prion study as well below)
following that are some other studies that may be of interest ;

 

 

 

Myiasis as a risk factor for prion diseases in humans

 

 

 

Journal of the European Academy of Dermatology and Venereology
Volume 20 Page 1037 - October 2006
doi:10.1111/j.1468-3083.2006.01595.x
Volume 20 Issue 9

 

REVIEW ARTICLE
Myiasis as a risk factor for prion diseases in humans
O Lupi *

 

Abstract

 

Prion diseases are transmissible spongiform encephalopathies of humans and
animals. The oral route is clearly associated with some prion diseases,
according to the dissemination of bovine spongiform encephalopathy (BSE or
mad cow disease) in cattle and kuru in humans. However, other prion diseases
such as scrapie (in sheep) and chronic wasting disease (CWD) (in cervids)
cannot be explained in this way and are probably more associated with a
pattern of horizontal transmission in both domestic and wild animals. The
skin and mucous membranes are a potential target for prion infections
because keratinocytes and lymphocytes are susceptible to the abnormal
infective isoform of the prion protein. Iatrogenic transmission of
Creutzfeldt–Jakob disease (CJD) was also recognized after corneal
transplants in humans and scrapie was successfully transmitted to mice after
ocular instillation of infected brain tissue, confirming that these new
routes could also be important in prion infections. Some ectoparasites have
been proven to harbour prion rods in laboratory experiments. Prion rods were
identified in both fly larvae and pupae; adult flies are also able to
express prion proteins. The most common causes of myiasis in cattle and
sheep, closely related animals with previous prion infections, are Hypoderma
bovis and Oestrus ovis, respectively. Both species of flies present a life
cycle very different from human myiasis, as they have a long contact with
neurological structures, such as spinal canal and epidural fat, which are
potentially rich in prion rods. Ophthalmomyiases in humans is commonly
caused by both species of fly larvae worldwide, providing almost direct
contact with the central nervous system (CNS). The high expression of the
prion protein on the skin and mucosa and the severity of the inflammatory
response to the larvae could readily increase the efficiency of transmission
of prions in both animals and humans.

 

 

International Journal of Dermatology
Volume 42 Page 425 - June 2003
doi:10.1046/j.1365-4362.2003.00345.x
Volume 42 Issue 6

 

Review
Could ectoparasites act as vectors for prion diseases?
Omar Lupi, MD, PhD
Abstract

 

Prion diseases are rare neurodegenerative diseases of humans and animals
with a lethal evolution. Several cell types found on the human skin,
including keratinocytes, fibroblasts and lymphocytes, are susceptible to the
abnormal infective isoform of the prion protein, which transforms the skin
to produce a potential target for prion infection. Iatrogenic transmission
of Creutzfeldt-Jakob disease was also recognized after corneal transplants
in humans, and scrapie was successfully transmitted to mice after ocular
instillation of infected brain tissue, confirming that these new routes, as
well as cerebral inoculation and oral ingestion, could be important in prion
infections. Animal prion infections, such as scrapie (sheep) and "mad cow
disease" (cattle), have shown a pattern of horizontal transmission in farm
conditions and several ectoparasites have been shown to harbor prion rods in
laboratory experiments. Fly larvae and mites were exposed to brain-infected
material and were readily able to transmit scrapie to hamsters. New lines of
evidence have confirmed that adult flies are also able to express prion
proteins. Because ocular and cerebral myiases and mite infestation are not
rare worldwide, and most cases are caused by fly larvae or hay mites that
usually affect sheep and cattle, it is important to discuss the possibility
that these ectoparasites could eventually act as reservoirs and/or vectors
for prion diseases.

 

 

 

 

P. tenuis – The White-tailed Deer Parasite

 

“Brain worms” (meningeal worms) can affect sheep, goats, llamas, alpacas,
moose and other exotic small ruminants

 

M. Kopcha, D.V.M., M.S., J. S. Rook, D.V.M. & D. Hostetler, D.V.M

 

MSU Extension & Ag. Experiment Station

 

Michigan State University

 

College of Veterinary Medicine

 

Many livestock producers are familiar with internal parasites that invade
the digestive system (the abomasum, small or large

 

intestines), liver, and lungs. An internal parasite which may not be so
well-recognized is one that invades the central nervous system

 

(brain and spinal cord). Commonly called the “brain worm” or meningeal worm
(the meninges are a thin membrane that covers the

 

brain and spinal column), the scientific name for this parasite is
Parelaphostroneylus tenuis (P. tenuis), and its natural host is the

 

White-tailed deer. Usually, P. tenuis completes its life cycle in

 

the deer (Figure 1) without causing noticeable problems.

 

However, when P. tenuis is ingested by unnatural, or aberrant

 

hosts such as, llamas, sheep, goats, moose, elk, caribou, and

 

other susceptible ruminants, the parasite moves into the brain

 

and/or spinal cord, damaging delicate nervous tissue.

 

Neurologic problems result.

 

White-tailed deer may he parasitized by P. tenuis year-round.

 

However, the neurologic disease seen in aberrant hosts has a

 

seasonal occurrence that starts in the late summer and continues

 

until a hard freeze occurs. A cool, moist summer and/or a mild

 

winter may extend the period during which the disease occurs.

 

How does it occur?

 

To understand this disease and how to prevent or minimize its

 

occurrence, it is important to understand the life cycle of P.

 

tenuis in the White-tailed deer and what happens when the

 

parasite is ingested by susceptible ruminants. The life cycle is

 

as follows (Figure 1): adult meningeal worms live in the deer's

 

central nervous system (brain and spinal cord) and produce

 

eggs which hatch into larvae. The larvae migrate from the deer's

 

central nervous system to the lungs, where they are coughed

 

into the mouth, swallowed and passed from the intestinal tract

 

with the manure. This portion of the life cycle takes

 

approximately three months (Figure 1 - numbers 1 and 2).

 

After excreted in the manure, larvae must continue their

 

development in an intermediate host (certain land-dwelling

 

snails and slugs) for another three to four weeks until they reach

 

their infective stage (Figure 1 - numbers 3 and 4).

 

White-tailed deer become infested with P. tenuis by eating

 

these snails or slugs that contain the infective stage of the larvae

 

(Figure 1 - number 5). Once ingested, the larvae migrate

 

through the deer’s gut and eventually move into their central

 

nervous system where they mature into adults, produce eggs,

 

Figure 2 The Angora goat in the

 

center of the picture had a mild

 

lameness in its left forelimb

 

(arrow). The presumptive

 

diagnosis was meningeal worm

 

infestation. Mild cases such as

 

this one may recover

 

spontaneously.

 

Figure 3 This Angora goat was

 

probably affected with

 

meningeal worms and was able

 

to use its hindlimbs, but was

 

unable to rise onto its

 

forelimbs.

 

Figure 4 This alpaca had been

 

paralyzed by meningeal worms.

 

Notice that despite the paralysis,

 

the animal appears alert. This is

 

typical for a brain worm

 

infestation that affects the spinal

 

cord and not the brain.

 

Figure 6: This Suffolk sheep was one of several

 

sheep from a flock that were affected with

 

Parelaphostrongylus tenuis. The posture that this

 

animal is displaying is referred to as a

 

“dogsitting” position.

 

Figure 5: This alpaca

 

displayed weakness in both

 

hindlimbs and was unable to

 

stand without assistance. The

 

presumptive diagnosis was

 

brain worm infestation. This

 

animal eventually recovered.

 

and the cycle begins again.

 

When P. tenuis-infected snails and slugs are ingested by aberrant hosts, the
larvae migrate into the brain and/or spinal cord, but

 

do not mature into adults. Instead, these immature larvae wander through the
central nervous system causing inflammation and

 

swelling which damages sensitive nervous tissue producing a variety of
neurologic signs. Because these larvae do not mature into

 

adults in aberrant hosts, they cannot produce eggs that would mature into
larvae which would then pass outside the animal with the

 

feces. This is why sheep, goats, llamas and other unnatural hosts are
considered dead-end hosts for P. tenuis. Dead end hosts

 

infected with P. tenuis larva cannot spread the disease to other aberrant
hosts or back to deer - i.e. infected sheep or

 

goats can not bring the disease to your flock or herd.

 

The neurologic signs observed in infected llamas,

 

sheep, goats and others depend upon the number of

 

larvae present in the nervous tissue and the specific

 

portion of the brain or spinal cord that has been

 

affected. For example - a mild infestation in a very

 

local area may produce a slight limp (Figure 2)) or

 

weakness in one or more legs (Figure 3,4,5, & 6). A

 

more severe infestation may cause an animal to

 

become partially or completely paralyzed. If the

 

parasites are located only in the spinal cord, an

 

affected animal will appear bright and alert, and have

 

a normal appetite, despite the altered gait or

 

paralysis. When larvae migrate through the brain, they

 

may cause blindness, a head tilt, circling, disinterest in

 

or inability to eat, or other signs that can mimic brain

 

diseases caused by bacteria, viruses, nutritional

 

deficiencies, trauma, or toxins. Table I lists some of

 

the diseases that P. tenuis can mimic when the

 

parasites migrate through nervous tissue.

 

Table 1_Included in this table are various diseases that can look similar to

 

“brain worm” infestation. Also listed are the target species that are

 

susceptible to each of the diseases.

 

Species

 

Disease Llamas and

 

Alpacas

 

Sheep Goats

 

Listeriosis X X X

 

Caprine Arthritis-

 

Encephalitis

 

X

 

Scrapie X Rare*

 

Rabies X X X

 

Trauma X X X

 

Copper Deficiency X X X

 

Vitamin E/Selenium

 

Deficiency

 

X X X

 

Spinal Cord or Brain

 

Abscess

 

X X X

 

Polioencephalomalacia X X X

 

Could it happen on my farm?

 

Animals pastured in lowland areas frequented by infected White-tailed deer
are prime candidates for exposure to snails containing

 

P. tenuis larvae. When such animals develop neurological problems during the
late summer through early winter in the Upper

 

Midwest (the season for exposure may be longer in other parts of the
country), “brain worms” are a likely possibility.

 

Presently there is no definitive test

 

that can be performed on a live

 

animal to confirm P. tenuis

 

infestation. Since the larvae do not

 

mature to adulthood in aberrant

 

hosts, and therefore, cannot

 

produce eggs or pass larvae in the

 

feces, a fecal examination is not

 

useful. Also, these parasites cannot

 

be detected by blood testing.

 

A test that can help support

 

suspicions of brain worm infestation

 

is evaluation of cerebrospinal fluid

 

(CSF), which is the fluid that

 

bathes the brain and spinal cord.

 

Disease that occurs in these areas

 

may cause changes in the CSF

 

detectable by various tests.

 

Normal CSF contains very few

 

cells and little protein. An animal

 

that has parasites migrating in the

 

brain or spinal cord, often will have

 

a larger number of cells, especially

 

a certain type of cell called an

 

eosinophil. Also, the protein

 

concentration may be increased.

 

Therefore, finding eosinophils in a

 

CSF tap taken from an animal with

 

neurologic abnormalities is very supportive evidence for “brain worm”
infestation. If eosinophils are not found, this does not rule

 

out the possibility of a “brain worm” problem. Currently, the only way to
confirm this diagnosis is by finding the parasite in the

 

nervous system, which requires a necropsy examination.

 

Obtaining CSF from sheep, goats, and llamas is somewhat more involved than
obtaining a blood sample. Two areas used most often

 

for CSF collection are just behind the poll or over the hips, in the area
called the lumbosacral junction. We prefer the lumbosacral

 

site because the test can be performed using local anesthetic only (rarely
would a tranquilizer be required), and the animal can be

 

standing or lying down, whichever is most comfortable. The head site usually
requires that the animal be heavily tranquilized or

 

anesthetized.

 

The procedure can be performed in a hospital setting or on the farm, and
must be done in a sterile manner. This includes removal

 

of the hair or wool from a small area where the puncture will be made,
scrubbing the site with surgical disinfectant and rinsing with

 

alcohol. Sterile gloves and equipment are used.

 

After the site has been scrubbed, an injection of a local anesthetic is
placed under the skin and into the deeper tissues where the

 

spinal needle will be placed. The needle is inserted through the
anesthetized area. The animal may notice slight discomfort when the

 

needle enters the spinal canal. However, having a quiet person at the
animal's head (in some cases the best person is the owner or

 

handler) will provide a calming effect. The needle does not penetrate the
spinal cord. In many animals, the cord ends just ahead of

 

where the needle is placed. Once fluid has been obtained, the needle is
withdrawn. The amount of fluid collected depends on the

 

animal's size. Usually, 5 to 8 cc's are withdrawn and submitted to a
clinical laboratory for analysis. This is a very safe procedure

 

if performed properly.

 

What about treatment?

 

Many different drugs including thiabendazole, levamisole, fenbendazole,
albendazole, and ivermectin have been used in an attempt

 

to treat “brain worm” infestation. However, to date, no controlled studies
have confirmed or refuted the efficacy of various treatment

 

recommendations. Some anthelmintics can kill P. tenuis larvae while they
migrate from the stomach to the brain or spinal cord, but

 

are unable to enter the central nervous system because of a structure called
the blood-brain barrier. Therefore, they do not have

 

an effect on parasitic larvae once the parasite has migrated across the
blood-brain barrier and is in the central nervous system. Other

 

anthelmintics may be able to kill the larvae regardless of their location in
the body. An important point to remember is that once the

 

parasite begins to migrate within the nervous tissue, damage occurs that is
usually irreversible. Although some drugs may kill the

 

worms, thus pre venting further damage, treatment does not repair nervous
tissue. Some animals with mild clinical signs may recover

 

without treatment. At this time, the best recommendation for treatment is
"do no harm." Perhaps some medications are helpful,

 

however, remember that drugs used at higher-than-usual levels or more
frequently than usual may cause toxicity problems.

 

The best approach to “brain worm” infestation is prevention. This s achieved
by keeping the life cycle in mind. Animals kept in

 

pastures that have wetlands and White-tailed deer should be removed from
these pastures in the late summer and until the first hard

 

freeze. If this is not possible, strategic deworming is the second best
approach. This would involve either continuously providing

 

an anthelmintic in feed or mineral mix throughout the “brain worm” season,
or deworming with an oral or injectable product every

 

10 to 14 days - starting in late summer and continuing through early to
mid-winter, depending on the severity of the freezing

 

temperatures.

 

The 10- to 14-day schedule recommendation is based on experimental evidence
that demonstrated the parasites' ability to reach

 

the brain and/or spinal cord in this amount of time after an animal eats the
snails containing P. tenuis larvae. Thus, this is a "window

 

of opportunity" to kill the worms before they enter the central nervous
system where they may be "safe" or protected from the killing

 

effect of drugs that cannot cross the blood-brain barrier.

 

While clinical cases of meningeal worm infestation are rare, “brain worms”
could affect your animals if they have access to wetlands

 

harboring P. tenuis-infected White-tailed deer. Wetlands contain a
population of snails and slugs needed to complete the parasite's

 

life cycle if it is the season when P. tenuis infestation occurs. Remember:
the success of treatment is variable - prevention is the best

 

means of control.

 

 

 

TSS

Is Texas hunting coming to an impasse?

 

By Jamie Svrcek
Correspondent  

 

Published June 8, 2007

 

Is the way that we hunt in Texas eventually leading to the downfall of the sport as we know it?

 

An article published in this month’s Field and Stream magazine gives new credibility to things that many have said about the way Texans hunt and points to the possibility of a ticking time bomb right under our noses.

 

That bomb comes in the form of chronic wasting disease, a spongiform encephalopathy that affects the cervid species. In laymen’s terms, it is the deer and elk version of mad cow disease.

 

As cited by “The quiet spread of CWD,” the said article in Field and Stream, by Jim Thornton, veterinarian Edward A. Hoover, a professor at Colorado State University and author of a forefront CWD study, points to the real danger of the disease being the way that it is spread — through the transmission of saliva, almost a surety under feeders and at mineral and salt licks.

 

While there are no known cases of CWD in Texas, you have to look a little deeper to see the potential danger to our deer herds. Captive herds are more likely to be infected than naturally free-ranging deer.

 

The problem is that, with the stocking practices that are in vogue on game ranches, there is also a huge lack of regulation to track where the animals are coming from.

 

Oftentimes, the ranchers who raise the deer that stock these game ranches fall in between the regulation of state livestock boards and state wildlife agencies and, just as often, lobby both sides of the fence to avoid the fees, regulation, documentation and other practices that cattlemen and herders must follow.

 

It’s easy to see that a couple of unscrupulous game managers and ranchers, driven by the potential money that goes along with the “trophy deer” hunt industry that has developed in the past few years, could easily ship deer from out of state and infect Texas herds.

 

And CWD is spreading. First discovered in Colorado in the 1960s, it has spread to 10 other states and not only in captive herds — it has also been found in wild deer.

 

According to a report from 2003 posted by Texas Parks and Wildlife, there is no way to test meat for CWD. The only way to test is by examination of brain and lymph-node tissue.

 

To further complicate this, the disease has been linked to nonliving proteins known as “prions”. These protein molecules do not die and can infect the ground where, say, an infected animal dies and decomposes.

 

It has been proven that, in captive herds, one infected animal can infect up to 80 percent of the rest of the herd.

 

It makes sense that, with this looming on the horizon, maybe it is time to change the course of hunting in Texas.

 

The notion of hunting feeders, especially with the present agri-techonology available for food plots, makes them obsolete.

 

Besides, it has been proven that deer benefit from year-round nutrition programs, both in terms of health and horn development.

 

That leaves one issue, high fencing. This is one issue that you either love or hate.

 

What many see is the classic case of a few benefiting at the possible expense of the rest of the state’s hunters.

 

Those who hunt fenced land point to the ease with which herds can be managed and the decreased possibility of poaching.

 

Outfitters like fencing because it makes it easier to put high-paying clients on the deer that they “want.”

 

From a biological standpoint, it seems to come down to one thing; when a land- or lease-owner puts up high fencing, he has just captured wild animals and in effect “domesticated” them.

 

It is an ethics issue after that for the most part, although for many it’s strictly a money issue, until you factor in problems such as CWD.

 

With it proven that captive herds are more susceptible to contracting CWD, wouldn’t it be easier to protect the deer population without adding these problems on top of it?

 

Until next week, I’ll see you “Out There.”

 

Jamie Svrcek is the outdoors columnist for The Daily News. Contact him at jamiesvrcek(at)gmail.com.

 

 

 

 

 

 

Subject: Infectious Prions in the Saliva and Blood of Deer with Chronic
Wasting Disease
Date: October 5, 2006 at 1:45 pm PST


Infectious Prions in the Saliva

and Blood of Deer with Chronic

Wasting Disease


Candace K. Mathiason,1 Jenny G. Powers,3 Sallie J. Dahmes,4 David A.
Osborn,5 Karl V. Miller,5

Robert J. Warren,5 Gary L. Mason,1 Sheila A. Hays,1 Jeanette Hayes-Klug,1
Davis M. Seelig,1

Margaret A. Wild,3 Lisa L. Wolfe,6 Terry R. Spraker,1,2 Michael W. Miller,6
Christina J. Sigurdson,1

Glenn C. Telling,7 Edward A. Hoover1*


A critical concern in the transmission of prion diseases, including chronic
wasting disease (CWD)

of cervids, is the potential presence of prions in body fluids. To address
this issue directly, we

exposed cohorts of CWD-nai¨ve deer to saliva, blood, or urine and feces from
CWD-positive deer.

We found infectious prions capable of transmitting CWD in saliva (by the
oral route) and in blood

(by transfusion). The results help to explain the facile transmission of CWD
among cervids and

prompt caution concerning contact with body fluids in prion infections.


SNIP...


Deer cohorts 1 (blood), 2 (saliva), and 3

(urine and feces) were electively euthanized at

18 months pi to permit whole-body examination

for PrPCWD. The greatest scrutiny was directed

toward those tissues previously established

to have highest frequency of PrPCWD deposition

in infected deer and generally regarded

as the most sensitive indicators of infection-

medulla oblongata and other brainstem regions,

tonsil, and retropharyngeal lymph node. We

found unequivocal evidence of PrPCWD in brain

and lymphoid tissue of all six tonsil biopsy-

positive deer in cohorts 1 (blood) and 2 (saliva),

whereas all deer in cohorts 3 and 5 were negative

for PrPCWD in all tissues (Table 2 and

Figs. 1 and 2).

The transmission of CWD by a single blood

transfusion from two symptomatic and one

asymptomatic CWDþ donor is important in at

least three contexts: (i) It reinforces that no tissue

from CWD-infected cervids can be considered

free of prion infectivity; (ii) it poses the

possibility of hematogenous spread of CWD,

such as through insects; and (iii) it provides a

basis for seeking in vitro assays sufficiently

sensitive to demonstrate PrPCWD or alternate

prion protein conformers in blood-one of the

grails of prion biology and epidemiology.

The identification of blood-borne prion

transmission has been sought before with mixed

results (9-11). Bovine spongiform encephalopathy

and scrapie have been transmitted to naBve

sheep through the transfer of 500 ml of blood

or buffy coat white blood cells from infected

sheep (12, 13). In addition, limited but compelling

evidence argues for the transmission of variant

Creutzfeldt-Jakob disease (vCJD) through blood

from asymptomatic donors (14-16). Even in

sporadic CJD, PrPres has been found in periph-

eral organs of some patients (17). The present

work helps establish that prion diseases can be

transmitted through blood.

The presence of infectious CWD prions in

saliva may explain the facile transmission of

CWD. Cervid-to-cervid interactions (SOM text),

especially in high density and captive situations,

would be expected to facilitate salivary crosscontact

(11, 18, 19). Salivary dissemination of

prions may not be limited to CWD. Proteaseresistant

prion protein has been demonstrated in

the oral mucosa, taste buds, lingual epithelium,

vomeronasal organ, and olfactory mucosa of

hamsters infected with transmissible mink

encephalopathy (19) and ferrets infected with

CWD (20). Although no instance of CWD

transmission to humans has been detected, the

present results emphasize the prudence of using

impervious gloves during contact with saliva or

blood of cervids that may be CWD-infected.

Environmental contamination by excreta

from infected cervids has traditionally seemed

the most plausible explanation for the dissemination

of CWD (21). However, we could not

detect PrPCWD in cohort 3 deer inoculated repeatedly

with urine and feces from CWDþ deer and examined up to 18 months pi (Table
2).

There are several reasons to view this negative

finding cautiously, including small sample size,

elective preclinical termination, and potential

variation in individual susceptibility that may

be associated with the 96 G/S polymorphism in

the PRNP gene (7, 22). Although no genotype

of white-tailed deer is resistant to CWD infection,

PRNP genotypes S/S or G/S at codon 96

appear to have reduced susceptibility manifest

by longer survival (7). Both deer in cohort 3

(urine and feces) were subsequently shown to

be of the PRNP 96 G/S genotype. Thus, it is

possible, although we think unlikely, that these

deer had a prolonged incubation period (918

months pi) before the amplification of PrPCWD

became detectable in tissues. Recent studies

have shown that PrPres is poorly preserved

after incubation with intestinal or fecal content

(23, 24). Further research using cervid and surrogate

cervid PrP transgenic mice (25) are indicated

to continue to address the presence of

infectious CWD prions in excreta of CWDþ deer and to provide a more
substantial basis for

reconsideration of the assumption that excreta

are the chief vehicle for CWDdissemination and

transmission.

The results reported here provide a plausible

basis for the efficient transmission of CWD in

nature. We demonstrate that blood and saliva in

particular are able to transmit CWD to naBve deer

and produce incubation periods consistent with

those observed in naturally acquired infections

(3, 26). The time from exposure to first detection

of PrPCWD by tonsil biopsy was variable-as

short as 3 months but as long as 18 months (likely

underestimates due to sampling frequency).

The results also reinforce a cautious view of the

exposure risk presented by body fluids, excreta,

and all tissues from CWDþ cervids. ...



SNIP...END


http://www.sciencemag.org/cgi/content/abstract/314/5796/133


Research

Environmental Sources of Prion Transmission in Mule Deer
Michael W. Miller,* Elizabeth S. Williams,† N. Thompson Hobbs,‡ and Lisa L.
Wolfe*
*Colorado Division of Wildlife, Fort Collins, Colorado, USA; †University of
Wyoming, Laramie, Wyoming, USA; and ‡Colorado State University, Fort
Collins, Colorado, USA

Suggested citation for this article: Miller MW, Williams ES, Hobbs NT, Wolfe
LL. Environmental sources of prion transmission in mule deer. Emerg Infect
Dis [serial on the Internet]. 2004 Jun [date cited]. Available from:
http://www.cdc.gov/ncidod/EID/vol10no6/04-0010.htm


----------------------------------------------------------------------------
----

Whether transmission of the chronic wasting disease (CWD) prion among
cervids requires direct interaction with infected animals has been unclear.
We report that CWD can be transmitted to susceptible animals indirectly,
from environments contaminated by excreta or decomposed carcasses. Under
experimental conditions, mule deer (Odocoileus hemionus) became infected in
two of three paddocks containing naturally infected deer, in two of three
paddocks where infected deer carcasses had decomposed in situ ˜1.8 years
earlier, and in one of three paddocks where infected deer had last resided
2.2 years earlier. Indirect transmission and environmental persistence of
infectious prions will complicate efforts to control CWD and perhaps other
animal prion diseases.

http://www.cdc.gov/ncidod/EID/vol10no6/04-0010.htm

Epidemiology of Chronic Wasting Disease in Captive White-Tailed
and Mule Deer
Michael W. Miller1,3 and Margaret A. Wild1,2 1 Colorado Division of
Wildlife, Wildlife Research Center, 317 West
Prospect Road, Fort Collins, Colorado 80526-2097, USA; 2 Current address:
National Park Service, Biological
Resource Management Division, 1201 Oak Ridge Drive, Suite 200, Fort Collins,
Colorado 80525, USA; 3 Corresponding
author (email: mike.miller@state.co.us)
ABSTRACT: The natural occurrence of chronic
wasting disease (CWD) in a 1993 cohort of captive
white-tailed deer (Odocoileus virginianus)
afforded the opportunity to describe epidemic
dynamics in this species and to compare dynamics
with those seen in contemporary cohorts
of captive mule deer (O. hemionus) also
infected with CWD. The overall incidence of
clinical CWD in white-tailed deer was 82%
(nine of 11) among individuals that survived
.15 mo. Affected white-tailed deer died or
were killed because of terminal CWD at age
49–76 mo (x¯559.6 mo, SE53.9 mo). Epidemic
dynamics of CWD in captive white-tailed deer
were similar to dynamics in mule deer cohorts.
Incidence of clinical CWD was 57% (4/7)
among hand-raised (HR) and 67% (4/6) among
dam-raised (DR) mule deer; affected HR mule
deer succumbed at 64286 mo of age (x¯572
mo; SE55 mo), and affected DR mule deer
died at age 31–58 mo (x¯541.3 mo; SE56.1
mo). Sustained horizontal transmission of
CWD most plausibly explained epidemic dynamics,
but the original source of exposures
could not be determined. Apparent differences
in mean age at CWD-caused death among
these cohorts may be attributable to differences
in the timing or intensity of exposure to CWD,
and these factors appear to be more likely to
influence epidemic dynamics than species differences.
It follows that CWD epidemic dynamics
in sympatric, free-ranging white-tailed
and mule deer sharing habitats in western
North American ranges also may be similar.


snip...


Captive mule deer held in what is now
the FWRF had been infected with CWD
since at least the late 1960s (Williams and
Young, 1992). After attempting to eradicate
CWD from the FWRF in 1985 by
killing all captive mule deer and elk and
cleaning the facility (Williams and Young,
1992; Miller et al., 1998), a new mule deer
research herd was started in 1990 with
nine animals (Miller and Williams, 2003).
This founder herd was augmented by natural
births and ‘‘orphan’’ fawns. Founders
and orphans were accepted only from outside
areas where CWD was known to be
endemic. Despite extensive preventive
measures, a case of CWD was diagnosed
in 1994 in a FWRF-born female from the
1991 cohort. This represented the beginning
of another CWD epidemic in captive
mule deer (Fig. 1), 8.5 yr after the last
infected deer had lived at FWRF.
White-tailed deer had not been held at
the FWRF site before 1993. In May–June
1993, 12 newborn white-tailed deer fawns
were captured by hand from the Rocky
Mountain Arsenal National Wildlife Refuge,
a fenced enclosure where surveys
conducted since 1993 have revealed no evidence
of CWD in resident deer populations
(Creekmore et al., 1999; Miller et al.,
2000; Miller and Williams, 2003; M. W.
Miller, unpubl.). After capture, fawns were
transported to FWRF. There, they were
held in dedicated rearing pens on the facility’s
east side, away from adult cervids.
Fawns were fed canned evaporated milk,
a pelleted feed, and alfalfa hay, using wellestablished
rearing protocols (Wild and
Miller, 1991). Eleven of 12 fawns (six females,
two males, and three castrated
males) survived until weaning, at which
time they were moved to a new paddock
(W) on the facility’s west side (Fig. 2A).
This new paddock, which had an electri-
fied perimeter fence, was in proximity to
other new deer paddocks and to older
paddocks but had not previously held deer
or elk. Weaned deer were maintained on
pelleted feed, alfalfa hay, and natural veg
etation consisting of forbs and grasses;
their diet was free from animal-derived
protein. Once they were sexually mature
(.12 mo old), the two males were moved
into an adjacent paddock (A) during November–
February each year, to prevent
breeding with females; this adjacent paddock
housed intact and castrated male
mule deer year round. Aside from occasional
research-related movements to handling
and weighing facilities and isolation
pens, female and castrated male whitetailed
deer resided in their primary paddock
throughout their respective lives.
Clinical signs suggestive of CWD
(weight loss, inattentiveness, and mild depression)
were first recorded in one male
and one castrated male white-tailed deer
in May 1997. By late June, both deer were
showing signs of end-stage CWD (emaciation,
pronounced behavioral changes,
ataxia, and ptyalism; Fig. 3), and both were
killed on 8 July. The other male began
showing clinical signs in late June; his condition
deteriorated rapidly, and he was
killed on 23 July after exhibiting an acute
onset of neurological signs, including opisthotonos.
A fourth deer, a female, was
found dead on 27 July after several days
of heavy rain and flooding at the FWRF;
CWD was diagnosed postmortem. In retrospect,
early signs of CWD (particularly
social isolation) had been present in this
fourth animal for ;1 mo. Four additional
deer were killed during end-stage CWD 9,
11, 23, and 26 mo after the index cases
(Fig. 4). By October 1999, because only
three white-tailed deer remained in the
herd, and one was showing signs of CWD,
the surviving deer were killed.
Chronic wasting disease was confirmed
in all nine clinical cases via histopathology
and immunohistochemistry (IHC), using
methods described elsewhere (Williams
and Young, 1993; Spraker et al., 1997;
Miller et al., 2000). Accumulations of
CWD-specific protease-resistant prion
protein (PrPCWD) were detected in multiple
sections of brain (particularly the medulla
oblongata, sectioned at the obex), in
tonsil, retropharyngeal lymph node, and
mesenteric lymph node tissues, and in
Peyer’s patches. Histological lesions of
spongiform encephalopathy described by
pathologists who evaluated these cases
were indistinguishable from those described
in free-ranging white-tailed deer
(Spraker et al., 1997; Williams and Miller,
2002); plaques composed of PrPCWD were
relatively consistent among these cases ....


PLEASE SEE FULL TEXT ;

http://wildlife.state.co.us/NR/rdonlyres/C82EB818-90C6-4D85-897E-9CE279546CCB/0/JWDEpiCWD.pdf


(13) CHRONIC WASTING DISEASE IN ELK (CERVUS ELAPHUS NELSONI)
HELD IN A CWD ENDEMIC FACILITY.
ELIZABETH S. WILLIAMS, Department of Veterinary Sciences, University of
Wyoming, Laramie, WY 82070; WALTER E. COOK, HANK EDWARDS, TERRY
KREEGER, Wyoming Game and Fish Department, Research Laboratory, Laramie, WY
82071; and SCOTT SMITH, Wyoming Game and Fish Department, Pinedale, WY
82941.
Fifty-seven female elk calves were captured on the National Elk Refuge,
Teton County,
Wyoming in February, 1995 and transported to the Sybille Wildlife Research
and
Conservation Education Unit near Wheatland, Wyoming. Chronic wasting disease
(CWD) is endemic in deer and elk in this facility. Chronic wasting disease
has never been
diagnosed in the Jackson Herd and tests of over 700 harvested adult elk have
been
negative. The elk calves were involved in a study of the efficacy of
Brucella abortus
strain RB51 vaccine; 33 were vaccinated by hand or ballistic implant. They
were held in
groups according to vaccination status in paddocks that had been used to
house cervids
for many years. These elk were not known to have had direct contact with elk
or deer
with CWD, though fence-line contact was possible. Between 19 and 28 months
after
moving into the facility, five elk developed clinical CWD. These animals had
spongiform
encephalopathy and were positive for accumulation of PrPres in the brain by
immunohistochemistry. As part of the vaccination trial protocol, the
remaining elk were
necropsied 27 to 31 months after moving to Sybille. Three of these elk had
spongiform
encephalopathy and were positive for PrP by immunohistochemistry and an
additional
three elk were positive by immunohistochemistry alone. Of the 54 elk that
lived for 1
year or more after introduction into the research facility, 11 (20%)
developed clinical or
subclinical CWD within 31 months. Exposure to the CWD prion apparently was
only
from environmental sources or possible fence- line contact with affected
cervids.


======================================


(14) MECHANISMS FOR CHRONIC WASTING DISEASE TRANSMISSION:
CLUES FROM INFORMATION-BASED COMPARISON OF COMPETING
TRANSMISSION MODELS.
MICHAEL W. MILLER, Colorado Division of Wildlife, Wildlife Research Center,
Ft.
Collins, CO.
Chronic wasting disease (CWD), a transmissible spongifom encephalopathy
(TSE),
occurs naturally in both captive and free-ranging deer (Odocoileus spp.) and
elk (Cervus
elaphus nelsoni). Although CWD is clearly a transmissible disease,
mechanisms
underlying its natural transmission remain undescribed. I used
information-based model
selection methods to compare four models for CWD transmission in mule deer
(O.
hemionus): maternal (dam-offspring) transmission; direct (lateral)
transmission without
latency; direct transmission with latency; and indirect (environmental)
transmission with
latency. Cumulative numbers of CWD cases forecast by each model were
compared to an
epidemic curve from a naturally-infected captive mule deer herd (n = 84
individuals)
maintained by the Colorado Division of Wildlife between June 1992 and May
2000. I
constrained parameter ranges and obtained maximum likelihood estimates of
relevant
parameters, then compared performance of respective models using Akaike's
information
criterion adjusted for small sample size (AICc). Of the models compared, the
indirect
transmission with latency model was strongly supported by epidemic data from
captive
mule deer (wr = 0.883). The direct transmission with latency model was only
marginally
supported by observed data (DAICc = 4.05, wr = 0.117), and the other two
models
enjoyed essentially no support from the data (wr * 3*10-7). Based on these
findings,
there appears to be a strong possibility that indirect transmission of CWD
via
contaminated environments occurs. It follows that indirect transmission
should be
considered in developing disease management strategies for both captive and
freeranging
cervids.





http://www.wildlifedisease.org/Documents/Proceedings/Wyoming_00.pdf


TSS

attitudes such as yours is what have decimated deer herds with this disease in many states that it was allowed to amplify and transmit through nothing more than ingorance and stupidity such as yours, so pop another top, and sit back and do nothing, and see what happens. if you love your hunt, and your deer, you will not take this disease so lightly. ...tss

attitudes such as yours is what have decimated deer herds with this disease in many states that it was allowed to amplify and transmit through nothing more than ingorance and stupidity such as yours, so pop another top, and sit back and do nothing, and see what happens. if you love your hunt, and your deer, you will not take this disease so lightly. ...tss

From:         "Terry S. Singeltary Sr."
Subject:      CWD UPDATE 88 AUGUST 31, 2007

Date:         Wed, 29 Aug 2007 21:13:08 -0500
From:         "Terry S. Singeltary Sr."
Subject:      CWD NEW MEXICO RECORDS IT'S 19 CASE (near Texas border again)

Monitoring the Potential Transmission of Chronic Wasting Disease to Humans Using a Hunter Registry Database in Wyoming (405 lines)
From: Terry S. Singeltary Sr. <[log in to unmask]>
Date: Thu, 30 Aug 2007 21:23:42 -0500

Subject: Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease
creates a new prion strain

Date: August 25, 2007 at 12:42 pm PST

Subject: Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease
creates a new prion strain
Date: August 25, 2007 at 12:42 pm PST

J Biol Chem. 2007 Aug 20; : 17709374

Cross-sequence transmission of sporadic Creutzfeldt-Jakob disease creates a
new prion strain.

[My paper] Atsushi Kobayashi , Masahiro Asano , Shirou Mohri , Tetsuyuki
Kitamoto

The genotype (methionine or valine) at polymorphic codon 129 of the human
prion protein (PrP) gene and the type (type 1 or type 2) of abnormal isoform
of PrP (PrP(Sc)) are major determinants of the clinicopathological
phenotypes of sporadic Creutzfeldt-Jakob disease (sCJD). Here we found that
transmission of sCJD prions from a patient with valine homozygosity (129V/V)
and type 2 PrP(Sc) (sCJD-VV2 prions) to mice expressing human PrP with
methionine homozygosity (129M/M) generated unusual PrP(Sc) intermediate in
size between type 1 and type 2. The intermediate type PrP(Sc) was seen in
all examined dura mater graft-associated CJD cases with 129M/M and
plaque-type PrP deposits (p-dCJD). p-dCJD prions and sCJD-VV2 prions
exhibited similar transmissibility and neuropathology, and the identical
type of PrP(Sc) when inoculated into PrP-humanized mice with 129M/M or
129V/V. These findings suggest that p-dCJD could be caused by cross-sequence
transmission of sCJD-VV2 prions.

snip...

In this study, the strain-dependent traits of sCJDMM1
prions were inherited through cross-sequence
transmission without any modification. The
humanized mice with 129V/V produced type 1 PrPres
after inoculation with sCJD-MM1 prions. Because
sCJD-VV1 cases are extremely rare (at most 1-2%
of the total number of sCJD cases) and characterized
by early onset (mean age at onset: 39.3 years) (5),

####################################

our results raise the possibility that CJD cases
classified as VV1 may include cases caused by
iatrogenic transmission of sCJD-MM1 prions or
food-borne infection by type 1 prions from animals,
e.g., chronic wasting disease prions in cervid. In fact,
two CJD-VV1 patients who hunted deer or
consumed venison have been reported (40, 41). The
results of the present study emphasize the need for
traceback studies and careful re-examination of the
biochemical properties of sCJD-VV1 prions.

###################################

In conclusion, cross-sequence transmission of
sCJD-VV2 prions generates a new prion strain with
altered conformational properties and disease
phenotypes as p-dCJD prions. Furthermore, the
newly generated prions have unique transmissibility
including the traceback phenomenon. In the future, if
atypical prion strains emerge through cross-sequence
transmission, especially from animals, traceback
studies will enable us to identify the origin of the
prions.

REFERENCES...snip...end

FULL TEXT ;

Re: Colorado Surveillance Program for Chronic Wasting Disease
Transmission to Humans (TWO SUSPECT CASES)

Terry S. Singeltary Sr.

P.O. Box 42

Bacliff, Texas USA 77518

What would happen if we did nothing to manage CWD?

Because there is no evidence of genetic resistance

to CWD in deer, the idea that it could simply “burn itself out” is nearly impossible. A simulation model suggests

that if left unmanaged over the next ten to thirty years, CWD will spread widely throughout Wisconsin and

increase in prevalence to more than 40 percent of adult deer. Colorado’s situation supports this model because

prevalence in mule deer on some local winter ranges there now exceeds 25-30 percent. To put this in perspective,

in some sections of Wisconsin’s core area prevalence is as high as 8-12 percent. In addition, the known affected

area of Colorado and Wyoming has expanded more than one hundred miles to the

west and northwest during the past five years.

Wildlife disease experts have concluded that in the absence of management intervention, CWD will most likely increase in prevalence and distribution. There is no evidence that CWD will “burn itself out” if left alone. A simulation model suggests that if left unmanaged over the next 10-30 years, CWD will spread quickly throughout Wisconsin and will substantially increase in prevalence to more than 40 percent of adult deer.
Simulations of effects on deer population size in the CWD affected area depend on the assumptions made about the transmission process, but all models show a moderate to substantial long-term reduction in deer population density. The model simulations are consistent with recent findings in Colorado that have shown increases in prevalence over the past few years in numerous local populations. Prevalence on some local winter ranges now exceeds 25-30 percent. In addition, the known affected area in both Colorado and Wyoming has expanded to the west and northwest more than 100 miles during the past five years.
 
http://www.dnr.state.wi.us/org/land/wildlife/whealth/issues/cwd/doc/ask06.htm#05
 
 
 
CWD INFECTION RATE OR STICKING YOUR HEAD IN THE SAND AND IGNORING
 
In one contaminated research facility, more than 90% of the deer housed for more than two years contracted CWD.

Such infection rates in wild deer populations would have devastating effects. .......

Northwestern Nebraska: In 2001, active surveillance in the vicinity of a CWD-positive

captive elk herd in Sioux County disclosed several infected white-tailed deer. On the

ranch with the positive elk, a CWD infection rate of approximately 50% was found

among 179 wild deer inside a high fence enclosure built on the property at the time the

elk enclosure was constructed in the early 1990s.

 DRAFT
WYOMING GAME AND FISH DEPARTMENT CHRONIC WASTING DISEASE MANAGEMENT PLAN
February 17, 2006

5. Predicted population effects on free-ranging elk based on captive elk chronically exposed to the CWD prion. Forty-three female elk calves were trapped at the National Elk Refuge and transported to Sybille in February 2002. Elk were housed in pens, assumed to be environmentally contaminated with the CWD prion. Elk will be held throughout their lifetimes. Elk dying will be examined and cause of death determined. From these data, it will should be possible to model free-ranging elk mortality and population dynamics under extreme circumstances of CWD prion exposure and transmission. As of December 2005 (46 months post capture), 11 of 43 elk have died due to CWD. This compares to 100% mortality in less than 25 months in elk orally inoculated with different dosages of the CWD prion.

Additionally, recent research indicates that there may be pockets of infection with very high rates of the CWD within the larger endemic area. Also, mature bucks appear to be infected at a higher rate than other portions of the population.

Upon learning that a number of captive whitetail taken inside the Sioux County game ranch tested CWD positive, and concerned about the Kimball County results, Commission staff in January 2002 began a culling operation within a 15-mile radius of the Sioux County game ranch. Of 113 wild animals taken in that culling operation, nine tested positive for the disease, for an overall infection rate of nearly eight percent. Of those testing positive, five were culled within two miles of the game ranch boundaries, two were culled within two to five miles, and two were culled within five to seven miles.

At the same time, Commission staff culled 172 mule and white-tailed deer from within the captive game ranch in Sioux County. Of 154 test results received, 79 animals tested positive. An additional culling, in cooperation with the South Dakota Department of Game, Fish and Parks, along our common border resulted in a sample size of 193 deer with all being negative.

In states where the disease has been present for more than a decade, the
prevalence of CWD in wild deer populations has been observed at 1%-15%. This rate, by itself, is not sufficient to cause
reductions in deer population size.
However, these observations occurred in states where deer populations do not achieve the high densities that occur in New
York and Wisconsin. In captive deer herds, CWD can reach remarkably high infection rates. In one contaminated research
facility, more than 90% of the deer housed for more than two years contracted CWD. Such infection rates in wild deer
populations would have devastating effects.
Hunting is the wildlife manager’s most important tool for regulating deer abundance. High deer population densities lead to
more rapid spread of CWD in an infected herd. Consequently, programs to reduce the deer population, which may include
increased harvest of female deer, will be implemented in areas where CWD has been detected.

Chronic wasting disease can reach remarkably
high prevalence in captive cervid populations.
In one infected research facility, more than 90%
of mule deer resident for more than 2 years died
or were euthanized while suffering from CWD.
Recently, high CWD prevalence (about 50%)
has been demonstrated in white-tailed deer
confined in association with an infected
Nebraska elk farm. Among captive elk, CWD
was the primary cause of adult mortality (5 of 7,
71%; 4 of 23, 23%) in 2 research herds, and
high prevalence (59%) was detected in a group
of 17 elk slaughtered from an infected farm
herd.
To estimate prevalence in infected free-ranging
populations, tissues from deer and elk harvested
by hunters in CWD-endemic areas have been
collected and examined at random. Within
endemic areas, prevalence of preclinical CWD
has been estimated at less than 1% in elk and
less than 1% to 15% in mule deer. Modeled
CWD epidemics failed to achieve a steady-state
equilibrium in infected deer populations,
suggesting that CWD may lead to local
extirpations of infected deer populations if left
unmanaged. (Excerpted and modified from:
Williams, Elizabeth S., Michael W. Miller, and
E. Tom Thorne. Chronic Wasting Disease:
Implications and Challenges for Wildlife
Managers. Transactions of the 67th North
American Wildlife and Natural Resources
Conference. In Press.)

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Monday, February 09, 2009