Parelaphostrongylus (Brainworm) Infection in Deer and Elk and the potential for CWD TSE prion consumption and spreading there from ?
Parelaphostrongylus (Brainworm) Infection in Deer and Elk and the potential
for CWD TSE prion consumption and spreading there from ?
Greetings everyone et al, and Merry Christmas,
I am hoping, and praying, that 2014 will bring forth much needed funding
for the TSE prion scientist around the globe.
I brought up a concern for a worm long ago, that gets in the brains of
cervids, and then the worm gets excreted via feces, and then deer forage and eat
that worm. if the host cervid of this worm has CWD, could this later transmit
CWD?
I was concerned about this long ago, still am. I was curious what any else
might think about this potential mode of transmission with cwd ?
there is much cwd risk factor now with soil, and now the potential exists
via plants, so I was just pondering out loud here, is it possible that some cwd
is being spread, by the Parelaphostrongylus (Brainworm), after sucking up on a
CWD infected cervids brain, and then being discarding via feces by that same CWD
infected cervid, soaking up the prions via the feces, laying in wait, for a CWD
free cervid to come scoop up and eat that Parelaphostrongylus (Brainworm), that
has been extremely exposed to the TSE prion ?
kind regards, terry
Parelaphostrongylus (Brainworm) Infection in Deer and Elk
Murray Woodbury DVM, MSc.
Specialized Livestock Research and Development Program
Department of Large Animal Clinical Sciences
Western College of Veterinary Medicine
University of Saskatchewn
Saskatoon,Saskatchewan S7N 5B4
Introduction
The parasite Parelaphostrongylus tenuis (P. tenuis) is also known as brain
worm, meningeal worm, Pneumostrongylus tenuis, Odocoileostrongylus tenuis,
Elaphostrongylus tenuis, or Neurofilaria cornellensis. Infection frequently
results in clinical disease called moose sickness, moose disease, moose
neurological disease, cerebrospinal parelaphostrongylosis, or cerebrospinal
nematodiasis. The existence of this parasite in eastern, but not western, North
America and the implications of it's movement west has severely affected live
animal trade in the farmed cervid industry of Canada. Etiology
Parelaphostrongylosis is caused by the roundworm, Parelaphostrongylus
tenuis. The major host for this parasite is the white-tailed deer where it is
carried without causing clinical signs of disease.
Geographic distribution
P. tenuis is present in eastern and central Canada including Nova Scotia,
New Brunswick, southern Quebec, Ontario, Manitoba, and eastern Saskatchewan (5).
It is also present in twenty eight of the eastern and central United States (1).
It is generally absent from coastal plains of the southeastern United States and
St. Croix of the Virgin Islands (14).
The parasite continues to spread extensively as white-tailed deer expand
their range in response to environmental changes such as deforestation,
agriculture and burning (5). Currently, the meningeal worm is not present in
western North America, however it is present in deer of the aspen parkland, and
there is no apparent barrier to its continued spread west toward the foothills
of the Rockies through such a corridor (5). Biologically, the meningeal worm
requires several criteria to be met for survival including the presence of
adequate numbers and overlapping populations of definitive (white-tail deer) and
intermediate hosts (terrestrial snails and slugs) in sufficient densities to
allow for establishment. It also needs a suitable climate for survival of
free-living stages of the parasites and suitable numbers of the hosts involved
(1). Ecologically, the prairie habitat and its dry conditions may affect the
survival of the first stage larvae and this may have some impact on controlling
the range of the nematode (9). In addition, the parasite is believed to be
associated with certain major soil types in combination with other environmental
attributes. However, what constitutes the barrier to generalized distribution is
unknown (4).
Prevalence
Prevalence of the meningeal worm ranges from less than 1% to greater than
85% throughout North America (1). Within Canada, the prevalence for adult worms
in the cranial cavities of deer are as follows: Manitoba 10%, Ontario 41- 61%,
Quebec 30%, New Brunswick 60%, and Nova Scotia 51% (1). The prevalence of
meningeal worms in aberrant hosts is generally unknown, however surveys have
been undertaken to determine the prevalence in such hosts (1).
Transmission
The life cycle of the meningeal worm is indirect with a typical prepatent
period of 82 to 91 days. However, the length may be inversely related to the
number of larvae ingested, and may be considerably longer in individual deer
(10). P. tenuis is a true lungworm in that it requires both a definitive host,
the white-tailed deer, and an intermediate host, a snail or slug. Deer become
infected by accidentally ingesting gastropods (snails) containing infective
third-stage larvae (L3) which are found on vegetation (4). Larvae are freed from
the gastropod tissue by digestion, and during the following ten days they
penetrate the abomasal wall, and migrate across the peritoneal cavity to gain
access to the central nervous system, likely through lumbar nerves (4). Once
they invade neural tissue, larval development occurs primarily in the dorsal
horns of the spinal cord. Fourth stage larvae (L4) emerge about 25 days after
initial ingestion (4). The L4 larvae leave the neural tissue and migrate to the
subdural space by day 40, after which they molt to the immature adult stage (4).
Once mature, some nematodes migrate to the venous sinuses of the cranium (4).
Some worms may deposit eggs on the meninges, but most deposit eggs directly into
the venous circulation where they are transported to the heart and lungs as
emboli (4). Eggs lodge in the lungs where they are incorporated into fibrous
nodules. These eggs embryonate into first-stage larvae (L1), move into the
alveoli, and up the bronchial escalator where they are coughed up and swallowed
to be excreted out in the mucous coat on the feces (4). The excreted L1
penetrate the foot of a terrestrial gastropod, where they grow and molt twice to
become the infective L3.
The time required for these two molts to occur is variable and highly
dependent on environmental conditions but it may be as short as three to four
weeks at summer temperatures. Larvae cease to develop when snails are
hibernating but development continues normally once snails become active (10).
Laboratory and field studies have shown that larvae are capable of overwintering
in the intermediate host (4).
Experimentally, a wide range of terrestrial gastropods may be infected,
however only a few species are generally involved in natural transmission. This
is likely related to preference of certain gastropods for favorable
microenvironments of forested areas with specific moisture content, evaporation,
and temperature (13). Commonly, gastropod availability in open meadows is less
than forested areas, reducing the likelihood of exposure to particular
gastropods for animals that utilize these areas to graze (13). Typically,
white-tailed deer spend most of their time in forested areas where gastropods
are found whereas elk spend most of their time in meadows and open fields (4).
Other equally important factors may include seasonal movement patterns in deer,
wapiti or gastropods, food preferences and selectivity for gastropods by the
host animal (13).
The early phase of the meningeal worm life cycle in aberrant hosts
parallels that in white-tailed deer, however the development of the larvae in
the central nervous system tends to produce neurologic signs and even death (4).
Meningeal worm larvae tend to be unusually active and damaging in neural tissue
of aberrant hosts. Some larvae fail to leave the neural parenchyma which results
in damage as the larvae matures and migrates, while other larvae invade the
ependymal canal or reinvade the spinal cord or brain after maturation (10). The
pathogenesis of the meningeal worm in fallow deer is different from other
cervids in that infective larvae penetrate the small intestine rather than the
abomasum (4).
Other species affected
A wide variety of species are susceptible to infection with P. tenuis,
namely, moose, elk, caribou, reindeer, mule deer, black-tailed deer, mule
deer/white-tailed deer hybrids, fallow deer, red deer, red deer/elk hybrids,
domestic sheep and goats, llamas, guinea pigs, and several bovid and cervid
species in zoos (1). It appears that reindeer, caribou, llamas, and domestic
goats are very susceptible to meningeal worm infection (1). It is speculated
that caribou and reindeer may be more likely to acquire infected gastropods
because of their feeding habits (4).
Clinical signs
The natural host for this infection is the white-tailed deer, and although
the parasite normally migrates to the meninges in this species, the deer
typically displays few clinical signs. Lack of apparent disease even with
neurological invasion has been attributed to the manner in which the larvae
reside in the neuropil of white-tail deer (4). In naturally and experimentally
infected white-tail deer, temporary lameness of the forelimb, circling, and
rapid oscillation of the eyeballs have been observed (1). Most white-tailed deer
survive infection without exhibiting clinical signs, however large larval
burdens could precipitate serious signs or even death.
In various cervids, camelids and other wild and domesticated ruminants,
very few P. tenuis larvae are required to produce a severe debilitating
neurological disease. The disease is expressed by locomotor incoordination,
lameness, stiffness, listlessness, progressive hindquarter weakness, circling,
abnormal position of the head and neck, blindness, and paralysis (1). Caribou
and reindeer also consistently exhibit exophthalmos or a "bug eyed" appearance
(4). Naturally infected elk become less wary, leave the herd and remain near
roads, fields or woodland clearings (14). Llamas infected with P. tenuis display
a sudden onset of weakness or ataxia and at least one of paraparesis
(generalized weakness), ataxia, exaggerated patellar reflexes, conscious
proprioceptive deficits (can't place feet correctly) or increased extensor tone
(rigid muscles) in the rear limbs (6). Cerebrospinal fluid aspirates in infected
llamas typically reveal increased protein and eosinophils (6). Fallow deer fawns
given high doses of infective larvae die sooner with signs associated with
severe peritonitis resulting from perforation of the intestinal wall, compared
to fawns given low doses of infective larvae which die later with signs
associated with paralysis and inability to rise (8). There is also a continuum
of responses to meningeal worm infection in elk: those exposed to large numbers
of infective larvae die; those exposed to low numbers survive, often without
infection; and those exposed to intermediate numbers often develop patent
non-fatal infections (9). Apparently, severity of clinical signs, resolution of
clinical signs and death are dose dependent.
Pathology
In white-tail deer, lesions associated with developing larvae are
relatively minor. Uncoiled larvae are generally located in cell-free tunnels in
the dorsal horns of the spinal cord surrounded by compressed neural tissue (4).
In white matter, scattered myelin sheath degeneration may be present, with
foreign body reactions around pieces of cuticle and hemorrhages associated with
larval migration, however, neural parenchyma quickly assumes a normal appearance
once larvae have left (4). Lesions associated with the adult meningeal worms in
the cranium are unremarkable (4). Lesions in the lungs consist of tiny
discolored spots uniformly distributed throughout the parenchyma and under the
pleura (10). Nodules may be found within the lungs due to a foreign-body
reaction that occurs around the remains of hatched eggshells (4). Congestion,
hemorrhages, and eosinophilic and lymphocytic infiltration is common in areas
where eggs or larvae have been in the lungs (4). Alveoli may collapse and
disappear resulting in subsequent fibrosis of the region which may show as
respiratory signs in naturally infected white-tailed deer (4).
Gross pathologic changes in infected aberrant host animals include
extensive central nervous system lesions including focal hemorrhages, neuronal
degeneration, tracking lesions in the brain and spinal cord, and yellowish
accumulations streaked with blood adjacent to the worms (1). Meningeal worms can
be found free in the cranial cavity or on the spinal cord or may be embedded in
nervous tissue (1).
As identified previously, larval penetration of the small intestine occurs
in fallow deer. It is believed that fallow deer are apparently unable to limit
the phase of nematode migration through the small intestine, even though they
are capable of mounting a substantial immune response against the meningeal worm
once it is within the central nervous system (4). This results in colitis and
fatal peritonitis, which is different than the pathology seen in all other
cervids (4). In fallow deer, the mucosa of the greater curvature of the abomasum
is hyperemic with scattered focal hemorrhages, the small intestine is filled
with black-red fluid, and the intestinal wall is slightly thickened with rugose
congested mucosae (8). Fibrinous adhesions are present throughout the peritoneal
cavity.
Microscopic lesions in aberrant hosts include small hemorrhages, masses of
parasite eggs, infiltrations of eosinophilic leukocytes, and congestion of very
small blood vessels (1). Additional microscopic lesions identified in llamas
include multifocal random areas of cavitation, axonal swelling, linear cavities
containing a variable number of lipid-laden macrophages and necrosis (6).
Diagnosis
Presently, the only definitive method for diagnosing P. tenuis infections
is recovery and identification of adult worms from the central nervous system at
necropsy (1).
The current diagnostic technique used in live animals is recovery of
first-staged larvae in feces or lung tissue using modified Baermann techniques.
Unfortunately, other protostrongylid nematodes shed similar cork-screw shaped
dorsal spiny-tailed larvae which may make it difficult to definitively identify
Parelaphostrongylus tenuis (1). Additionally, the first-stage larvae of P.
tenuis are resistant to dessication and freezing (4) and may be readily washed
off feces by water or rain (10) making it difficult to recover larvae using this
method. Detection of low-levels of infection by this method is complicated by
the parasite's long reproductive period which necessitates repeated testing of
feces from suspected animals for several months. It is known that the number of
larvae shed fluctuates by season with more larvae shed in winter-spring than in
summer-autumn and the normal host, the white-tailed deer, tends to shed more
larvae than the aberrant hosts such as elk (1). Also, animals infected with only
one worm, or worms of the same gender, will not shed larvae (12). It is also
possible that immunological factors and age of the host may play a role in the
levels of larval shedding (1).
Attempts to diagnose P. tenuis by measuring total protein concentration and
enzyme activity within the cerebrospinal fluid of domestic goats and
white-tailed deer showed inconclusive results (7). It is clear that
parelaphostrongylosis is accompanied by seroconversion, and that both species
develop a significant antibody response in cerebrospinal fluid, however the
inability to detect antibodies during the prepatent period hinders the
application of this technique as a diagnostic aid (7).
A primary objective of a study undertaken in 1996 was to develop simple and
reliable blood tests to detect meningeal worm infection in game-farmed animals
(3). The blood tests were based on the reaction between unique somatic antigens
to P. tenuis located in or on the worm to antibodies from the blood of infected
animals (3). A unique 37 kDa antigen of the third-stage larva, which is also
present in adult P. tenuis, serves as a serodiagnostic antigen to develop an
enzyme-linked immunosorbent assay as a reliable diagnostic test for P. tenuis
infection in white-tailed deer (12). However, the use of native 37kDa antigens
from either L3 or adults for developing serological tests is impractical because
the antigen is in low concentration in the parasite and would be difficult to
obtain. (12) Currently the antigen is being cloned and expressed using
recombinant DNA technology (12). Serological diagnosis of P. tenuis should offer
many advantages over the currently used method of fecal analysis (12),
especially with respect to differentiation of P. tenuis from other
protostrongylids.
Differential diagnoses
P. tenuis can be confused with other neurological disorders such as trauma,
brain abscesses, tumors, tick paralysis, listeriosis, degenerative myelopathy,
rabies and other parasites that cause cerebrospinal nematodiasis. Copper
deficiency may cause progressive ataxia, and chronic capture myopathy may have
external manifestations similar to some stages of P. tenuis infection (11).
Treatment
There are no drugs known to be effective against meningeal worms once they
invade the central nervous system (1).
Kocan treated deer with 0.1 mg/kg of ivermectin subcutaneously at 1, 10 and
30 days after exposure to meningeal worm larvae and only prevented infection in
deer treated 1 day after exposure (2). Once the larvae emerge from the
gastrointestinal tract and enter the central nervous system by six days
post-exposure, ivermectin has no effect because it does not readily cross the
blood brain barrier except at very high dosages (2). Larvae still penetrating
the abomasum, however, are readily killed (2). Treatment of deer with mature
worms reduces the number of larvae shed in feces, indicating that ivermectin is
effective against first-stage larvae in the lungs and perhaps on egg production
or viability, however live adult worms still persist in the central nervous
system (2).
According to masters thesis work by Sikarskie at Michigan State University,
limited clinical trials of the use of oral albendazole feed at 25 mg/kg in the
feed for two weeks, killed adult worms in the meninges of white-tailed deer
(11).
Llamas infected with P. tenuis have been treated with anthelmintics
including ivermectin and fenbendazole to kill the larval stages of the parasite
and anti-inflammatory drugs such as flunixin, phenylbutazone or dexamethasone to
decrease the inflammation in the neural tissue associated with migrating or dead
larvae (6). In all instances, the animals deteriorated and required euthanasia
in spite of treatment.
Control
Prevention of pasture contamination by white-tailed deer, and mollusk
management are the recommended procedures for controlling P. tenuis in wild
populations of white-tailed deer (4, 11). Control of the gastropod intermediates
is not feasible nor practical because gastropods are present in a wide variety
of environmental locations not readily reached by non-specific molluscicides and
would not be desirable because gastropods are very important to the ecosystem
(10). Controlling the nematode in the definitive host is also not a viable
option because there are no known drugs effective against P. tenuis, and
anthelmintic treatment of wild populations is generally not feasible (10).
Double fencing and establishment of a sanitary central region, cordon sanitaire,
has been used in quarantine stations to prevent access of either white-tailed
deer or gastropods (11). The ground of the cordon sanitaire must be regularly
harrowed or ploughed to keep it free of vegetation, with periodic application of
molluscicides to prevent gastropod migration (11).
Significance
The geographical distribution of P. tenuis is very important to wildlife
officials and game farm producers because it can cause significant mortality
among cervids. It has been suggested that parelaphostrongylosis may be
responsible for the decline of moose in some areas of the United States and
Canada and is a major factor preventing the establishment of moose, elk, and
caribou in areas populated by white-tailed deer (14). Presently, P. tenuis, is
considered the greatest threat to game farm animals and provincial wildlife
populations if it is accidentally introduced into Saskatchewan populations (1).
Concern centers on the potential for translocating and establishing the parasite
in nonendemic areas as a result of natural range expansion or translocation of
infected hosts (4). Research has illustrated that the meningeal worm can
successfully complete its life cycle in elk and that the larvae from such
infections are viable and can serve as a source for subsequent infections in
white-tailed deer and other elk (9). Current recommendations are that until
reliable diagnostic procedures are available, importation of game species from
areas where the parasite occurs should not occur (1). One must recognize that
should the meningeal worm be introduced into an area free from the disease, it
will be extremely difficult, if not impossible, to eradicate (1).
In order to establish quarantine protocols, research would need to be
conducted to determine when and how frequently fecal sampling (1) or serological
testing would need to be done. Contaminated enclosures used for holding
ungulates would need to be kept free of white-tailed deer for a least one to two
years and perimeter fences would need to be free of vegetation that could harbor
gastropods which could travel into the pens to infect the enclosed animals (10).
Even if the worm did not cause devastation to common native species it
would likely have a tremendous economic impact because of mortality, morbidity,
responses to public inquiry, lost natural resources and potential threats to the
domestic animal industry (1). Domestic goats appear to be exquisitely sensitive,
often dying within a few days of infection, while sheep are considerably less
susceptible (10). It is believed that cattle are one of the most resistant of
the domestic species, although meningeal worms have been recovered from the
central nervous system of healthy individuals and adult worms may reach the CNS
before the cattle die (10). Although the role of aberrant hosts in sustaining P.
tenuis populations or their role in translocating the parasite is not currently
known, introduction of this parasite to domestic farms could have a substantial
economic impact.
There is no indication that this parasite poses a risk to humans because it
is not infective to humans and meat of infected animals is safe for human
consumption (14).
Future research According to W.M. Samuel at the University of Alberta, a
variety of questions need to be answered in relation to this parasite (1). These
include: Do free-ranging elk in eastern North America shed larvae in their
feces? What are the specific boundaries of the meningeal worm distribution and
what mechanisms delineate this geographic distribution? How susceptible are
various native wild and domestic hosts to the meningeal worm? Hopefully, the
answers to these questions will soon become clear and with the development of
effective diagnostic tests Parelaphostrongylus tenuis infections will be readily
prevented, treated or controlled.
References
1.The review of wildlife disease status in game animals in North America,
Saskatchewan Game Farmers Association and The Saskatchewan Game Farming
Technical Advisory Committee, 1992. 2.Kocan AA. The use of ivermectin in the
treatment and prevention of infection with Parelaphostrongylus tenuis
(Dougherty) (Nematoda: Metastrongyloides) in white-tailed deer (Odocoileus
virginianus Zimmerman). Journal of Wildlife Diseases 1985; 21(4): 454-455.
3.Development of blood tests for Elaphostrongylus cervi and Parelaphostrongylus
tenuis in game-farmed animals. Agriculture Development Fund. 1996. Agriculture
and Agri-Food Canada. 4. Fowler ME, Miller RE. Zoo & Wild Animal Medicine
Current Therapy 4. Philadelphia: W. B. Saunders, 1999. 5. Bindernagel JA,
Anderson RC. Distribution of the meningeal worm in white-tailed deer in Canada.
Journal of Wildlife Management 1972; 36(4): 1349 - 1353. 6.Scarratt WK,
Karzenski SS, Wallace MA, et al. Suspected Parelaphostrongylosis in five llamas.
Progress in Veterinary Neurology 1996; 7(4): 124 - 129. 7.Dew TL, Bowman, DD,
Grieve RB. Parasite-specific immunoglobulin in the serum and cerebrospinal fluid
of white-tailed deer (Odocoileus virginianus) and goats (Capra hircus) with
experimentally induce parelaphostrongylosis. Journal of Zoo and Wildlife
Medicine 1992; 23:281 - 287. 8.Pybus MJ, Samuel WM, Welch DA, et al. Mortality
of fallow deer (Dama dama) experimentally infected with meningeal worm,
Parelaphostrongylus tenuis. Journal of Wildlife Diseases 1992; 28(1): 95 - 101.
9.Samuel WM, Pybus MJ, Welch DA, Wilke CJ. Elk as a potential host for meningeal
worm:implications for translocation. Journal of Wildlife Management 1992; 56(4):
629 - 639. 10.Davidson WR, Hayes FA, Nettles VF, et al. Lungworms (Anderson RC,
Prestwood AK) In Diseases and Parasites of White-tailed Deer. Tallahassee: Tall
Timbers Research Station,1981. 11.Haigh JC, Hudson RJ. Farming Wapiti and Red
Deer. St. Louis: Mosby, 1993. 12.Ogunremi O, Lankester M, Kendall J, Gajadhar A.
Serological diagnosis of Parelaphostrongylus tenuis infection in white-tailed
deer and identificiation of a potentially unique parasite antigen. Journal of
Parasitology; 85(1): 122 - 127. 13.Raskevitz RF, Kocan AA, Shaw JH. Gastropod
availability and habitat utilization by wapiti and white-tailed deer sympatric
on range enzootic for meningeal worm. Journal of Wildlife Diseases 1991; 27(1):
92 - 101. 14.http://www.dnr.state.mi.us/Wildlife/Divi...Publications/Disease_Manual/BRAINWM.html
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 scrapie infected 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 post inoculation, 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 post inoculation 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.
DECEMBER 2014 UPDATE
P.121: Efficient transmission of prion disease through environmental
contamination
Sandra Pritzkow, Rodrigo Morales, and Claudio Soto Mitchell Center for
Alzheimer’s disease and related Brain disorders; University of Texas Medical
School at Houston; Hourston, TX USA
Chronic wasting disease (CWD) is a prion disorder effecting captive and
free-ranging deer and elk. The efficient propagation suggests that horizontal
transmission through contaminated environment may play an important role. It has
been shown that infectious prions enter the environment through saliva, feces,
urine, blood or placenta tissue from infected animals, as well as by carcasses
from diseased animals and can stay infectious inside soil over several
years.
We hypothesize that environmental components getting in contact with
infectious prions can also play a role for the horizontal transmission of prion
diseases. To study this issue, surfaces composed of various environmentally
relevant materials were exposed to infectious prions and the attachment and
retention of infectious material was studied in vitro and in vivo. We analyzed
polypropylene, glass, stainless steel, wood, stone, aluminum, concrete and brass
surfaces exposed to 263K-infected brain homogenate. For in vitro analyses, the
material was incubated in serial dilutions of 263K-brain homogenate, washed
thoroughly and analyzed for the presence of PrPSc by PMCA. The results show that
even highly diluted PrPSc can bind efficiently to polypropylene, stainless
steel, glass, wood and stone and propagate the conversion of normal prion
protein. For in vivo experiments, hamsters were ic injected with implants
incubated in 1% 263K-infected brain homogenate. Hamsters, inoculated with
263K-contaminated implants of all groups, developed typical signs of prion
disease, whereas control animals inoculated with non-contaminated materials did
not.
In addition, in order to study the transmission in a more natural setting,
we exposed a group of hamster to habit in the presence of spheres composed of
various materials that were pretreated with 263K prions. Many of the hamsters
exposed to these contaminated materials developed typical signs of the disease
that were confirmed by immunohistological and biochemical analyses.
These findings suggest that various surfaces can efficiently bind
infectious prions and act as carriers of infectivity, suggesting that diverse
elements in the environment may play an important role in horizontal prion
transmission.
P.146: Kinetics and cell association of chronic wasting disease prions shed
in saliva and urine of white-tailed deer
Nicholas J Haley,1,2 Scott Carver,3 Clare E Hoover,1 Kristen A Davenport,1
Candace K Mathiason,1 Glenn C Telling,1 and Edward A Hoover1
1Department of Microbiology, Immunology, and Pathology, College of
Veterinary Medicine and Biomedical Sciences; Colorado State University; Fort
Collins, CO USA; 2Department of Diagnostic Medicine and Pathobiology, College of
Veterinary Medicine; Kansas State University; Manhattan, KS USA; 3School of
Zoology; University of Tasmania; Hobart, Tasmania, Australia
Chronic wasting disease, a transmissible spongiform encephalopathy (TSE) of
deer, elk, and moose, is unique among prion diseases in its relatively efficient
horizontal transmissibility. Recent studies have shown that excreta—saliva,
urine, and feces—from CWD-positive cervids may play an important role in
horizontal transmission of CWD, and although the precise onset of shedding in
these excreta is unknown, it is thought to occur long before the onset of
clinical symptoms. High levels of prion seeding activity have been demonstrated
in excretory tissues of deer, including tongue, salivary glands, kidney, and
urinary bladder, though the origin(s) and cellular nature of infectious prions
in excreta is unknown. We hypothesized that excretory shedding of CWD prions in
saliva and urine would coincide with the appearance of PrPd appearance in
peripheral lymphatic tissues, and that infectivity would associate with cellular
preparations of these excreta. Following intracerebral inoculation of
susceptible Tg[CerPrP] mice, we observed efficient transmission in saliva
collected as early as 12 months post-exposure, coinciding with peripheral PrPd
appearance in tonsil biopsies; while urine collected at terminal disease was
only minimally infectious in transgenic mice. We also found that acellular
preparations of saliva, and cellular preparations of urine, were capable of
transmitting CWD infection to transgenic Tg[CerPrP] mice with incubation periods
similar to that of whole saliva or urine; saliva and urine from CWD-negative
deer failed to induce prion disease in these mice. Infectious titers were
determined for obex and bodily fluids, and were similar to those previously
described. These findings extend our understanding of CWD shedding in
white-tailed deer, and offer insight into the source and cellular associations
of infectious CWD prions in excreta.
P.178: Longitudinal quantitative analysis of CWD prions shed in saliva of
deer
Davin M Henderson, Nina Garbino, Nathaniel D Denkers, Amy V Nalls, Candace
K Mathiason, and Edward A Hoover Prion Research Center, College of Veterinary
Medicine and Biomedical Sciences, Colorado State University; Fort Collins, CO
USA
Background/Introduction. Chronic Wasting Disease (CWD) is an emergent
rapidly spreading fatal prion disease of cervids (deer, elk and moose). CWD has
now been identified in 22 States (including two new states within the last
year), 2 Canadian provinces, and South Korea. Shedding of infectious prions in
excreta (saliva, urine, feces) may be an important factor in CWD transmission.
Here we apply an adapted version of a rapid in vitro assay [real-time
quaking-induced conversion (RT-QuIC)] to determine the time of onset, length,
pattern, and magnitude of prion shedding in saliva of infected deer.
Materials and Methods. The RT-QuIC assay was performed as previously
described in Henderson et al. PLoS-One (2013). Saliva samples were quantitated
by comparison to a RT-QuIC reaction rate standard curve of a bioassayed obex
sample from a terminally ill cervid.
Results. To better understand the onset and length of CWD prion shedding we
analyzed >150 longitudinally collected, blinded, then randomized saliva
samples from 17 CWD-infected and 3 uninfected white-tailed deer. We observed
prion shedding, as detected by the RT-QuIC assay, as early as 3 months from
inoculation and sustained shedding throughout the disease course in both aerosol
and orally exposed deer. We estimated the infectious lethal dose of prions shed
in saliva from infected deer by comparing real-time reaction rates of saliva
samples to a bioassayed serially diluted brain control. Our results indicate
that as little as 1 ml of saliva from pre-symptomatic infected deer constitutes
a lethal CWD prion dose.
Conclusions. During the pre-symptomatic stage of CWD infection and
throughout the course of disease deer may be shedding multiple LD50 doses per
day in their saliva. CWD prion shedding through saliva and excreta may account
for the unprecedented spread of this prion disease in nature. Acknowledgments.
Supported by NIH grant RO1-NS-061902 and grant D12ZO-045 from the Morris Animal
Foundation.
*** We conclude that TSE infectivity is likely to survive burial for long
time periods with minimal loss of infectivity and limited movement from the
original burial site. However PMCA results have shown that there is the
potential for rainwater to elute TSE related material from soil which could lead
to the contamination of a wider area. These experiments reinforce the importance
of risk assessment when disposing of TSE risk materials.
*** The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
PRION 2014 CONFERENCE
CHRONIC WASTING DISEASE CWD
A FEW FINDINGS ;
Conclusions. To our knowledge, this is the first established experimental
model of CWD in TgSB3985. We found evidence for co-existence or divergence of
two CWD strains adapted to Tga20 mice and their replication in TgSB3985 mice.
Finally, we observed phenotypic differences between cervid-derived CWD and
CWD/Tg20 strains upon propagation in TgSB3985 mice. Further studies are underway
to characterize these strains.
We conclude that TSE infectivity is likely to survive burial for long time
periods with minimal loss of infectivity and limited movement from the original
burial site. However PMCA results have shown that there is the potential for
rainwater to elute TSE related material from soil which could lead to the
contamination of a wider area. These experiments reinforce the importance of
risk assessment when disposing of TSE risk materials.
The results show that even highly diluted PrPSc can bind efficiently to
polypropylene, stainless steel, glass, wood and stone and propagate the
conversion of normal prion protein. For in vivo experiments, hamsters were ic
injected with implants incubated in 1% 263K-infected brain homogenate. Hamsters,
inoculated with 263K-contaminated implants of all groups, developed typical
signs of prion disease, whereas control animals inoculated with non-contaminated
materials did not.
Our data establish that meadow voles are permissive to CWD via peripheral
exposure route, suggesting they could serve as an environmental reservoir for
CWD. Additionally, our data are consistent with the hypothesis that at least two
strains of CWD circulate in naturally-infected cervid populations and provide
evidence that meadow voles are a useful tool for CWD strain typing.
Conclusion. CWD prions are shed in saliva and urine of infected deer as
early as 3 months post infection and throughout the subsequent >1.5 year
course of infection. In current work we are examining the relationship of
prionemia to excretion and the impact of excreted prion binding to surfaces and
particulates in the environment.
Conclusion. CWD prions (as inferred by prion seeding activity by RT-QuIC)
are shed in urine of infected deer as early as 6 months post inoculation and
throughout the subsequent disease course. Further studies are in progress
refining the real-time urinary prion assay sensitivity and we are examining more
closely the excretion time frame, magnitude, and sample variables in
relationship to inoculation route and prionemia in naturally and experimentally
CWD-infected cervids.
Conclusions. Our results suggested that the odds of infection for CWD is
likely controlled by areas that congregate deer thus increasing direct
transmission (deer-to-deer interactions) or indirect transmission
(deer-to-environment) by sharing or depositing infectious prion proteins in
these preferred habitats. Epidemiology of CWD in the eastern U.S. is likely
controlled by separate factors than found in the Midwestern and endemic areas
for CWD and can assist in performing more efficient surveillance efforts for the
region.
Conclusions. During the pre-symptomatic stage of CWD infection and
throughout the course of disease deer may be shedding multiple LD50 doses per
day in their saliva. CWD prion shedding through saliva and excreta may account
for the unprecedented spread of this prion disease in nature.
see full text and more ;
Monday, June 23, 2014
*** PRION 2014 CONFERENCE CHRONIC WASTING DISEASE CWD
NEW URL
*** Infectious agent of sheep scrapie may persist in the environment for at
least 16 years***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3
New studies on the heat resistance of hamster-adapted scrapie agent:
Threshold survival after ashing at 600°C suggests an inorganic template of
replication
Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel
Production
Detection of protease-resistant cervid prion protein in water from a
CWD-endemic area
NEW URL
A Quantitative Assessment of the Amount of Prion Diverted to Category 1
Materials and Wastewater During Processing
Rapid assessment of bovine spongiform encephalopathy prion inactivation by
heat treatment in yellow grease produced in the industrial manufacturing process
of meat and bone meals
http://transmissiblespongiformencephalopathy.blogspot.com/2013/07/rapid-assessment-of-bovine-spongiform.html
Survival and Limited Spread of TSE Infectivity after Burial
Karen Fernie, Allister Smith and Robert A. Somerville The Roslin Institute
and R(D)SVS; University of Edinburgh; Roslin, Scotland UK
Scrapie and chronic wasting disease probably spread via environmental
routes, and there are also concerns about BSE infection remaining in the
environment after carcass burial or waste 3disposal. In two demonstration
experiments we are determining survival and migration of TSE infectivity when
buried for up to five years, as an uncontained point source or within bovine
heads. Firstly boluses of TSE infected mouse brain were buried in lysimeters
containing either sandy or clay soil. Migration from the boluses is being
assessed from soil cores taken over time. With the exception of a very small
amount of infectivity found 25 cm from the bolus in sandy soil after 12 months,
no other infectivity has been detected up to three years. Secondly, ten bovine
heads were spiked with TSE infected mouse brain and buried in the two soil
types. Pairs of heads have been exhumed annually and assessed for infectivity
within and around them. After one year and after two years, infectivity was
detected in most intracranial samples and in some of the soil samples taken from
immediately surrounding the heads. The infectivity assays for the samples in and
around the heads exhumed at years three and four are underway. These data show
that TSE infectivity can survive burial for long periods but migrates slowly.
Risk assessments should take into account the likely long survival rate when
infected material has been buried.
The authors gratefully acknowledge funding from DEFRA.
Sunday, November 3, 2013
*** Environmental Impact Statements; Availability, etc.: Animal Carcass
Management [Docket No. APHIS-2013-0044] ***
Singeltary submission ;
Program Standards: Chronic Wasting Disease Herd Certification Program and
Interstate Movement of Farmed or Captive Deer, Elk, and Moose
DOCUMENT ID: APHIS-2006-0118-0411
***Singeltary submission
Docket No. 00-108-10 Chronic Wasting Disease Herd Certification Program and
Interstate Movement of Farmed or Captive Deer, Elk, and Moose; Program
Standards
>>>The CWD herd certification program is a voluntary, cooperative
program that establishes minimum requirements for the interstate movement of
farmed or captive cervids, provisions for participating States to administer
Approved State CWD Herd Certification Programs, and provisions for participating
herds to become certified as having a low risk of being infected with
CWD<<<
Greetings USDA/APHIS et al,
I kindly would like to comment on Docket No. 00-108-10 Chronic Wasting
Disease Herd Certification Program and Interstate Movement of Farmed or Captive
Deer, Elk, and Moose; Program Standards.
I believe, and in my opinion, and this has been proven by scientific facts,
that without a validated and certified test for chronic wasting disease cwd,
that is 100% sensitive, and in use, any voluntary effort will be futile. the
voluntary ban on mad cow feed and SRMs have failed terribly, the bse mad cow
surveillance program has failed terribly, as well as the testing for bse tse
prion in cattle, this too has failed terrible. all this has been proven time and
time again via OIG reports and GOA reports.
I believe that until this happens, 100% cwd testing with validated test,
ALL MOVEMENT OF CERVIDS BETWEEN STATES MUST BE BANNED, AND THE BORDERS CLOSED TO
INTERSTATE MOVEMENT OF CERVIDS. there is simply to much at risk.
In my opinion, and the opinions of many scientists and DNR officials, that
these so called game farms are the cause of the spreading of chronic wasting
disease cwd through much negligence. the game farms in my opinion are not the
only cause, but a big factor. I kindly wish to submit the following to show what
these factors are, and why interstate movement of cervids must be banned.
...
snip...see full text and PDF ATTACHMENT HERE ;
Tuesday, December 16, 2014
Evidence for zoonotic potential of ovine scrapie prions Scrapie from sheep
could infect humans with 'mad cow disease', study finds
http://transmissiblespongiformencephalopathy.blogspot.com/2014/12/evidence-for-zoonotic-potential-of.html
http://scrapie-usa.blogspot.com/2014/12/scrapie-from-sheep-could-infect-humans.html
Tuesday, December 16, 2014
Texas 84th Legislature 2015 H.R. No. 2597 Kuempel Deer Breeding Industry
TAHC TPWD CWD TSE PRION
Friday, February 08, 2013
*** Behavior of Prions in the Environment: Implications for Prion Biology
Uptake of Prions into Plants
Friday, August 09, 2013
***CWD TSE prion, plants, vegetables, and the potential for environmental
contamination
Friday, December 06, 2013 2:39 PM
Procedures for identifying infectious prions after passage through the
digestive system of an avian species
Saturday, March 10, 2012
CWD, GAME FARMS, urine, feces, soil, lichens, and banned mad cow protein
feed CUSTOM MADE for deer and elk
PRION2013 CONGRESSIONAL ABSTRACTS CWD
Sunday, August 25, 2013
***Chronic Wasting Disease CWD risk factors, humans, domestic cats, blood,
and mother to offspring transmission
Sunday, July 21, 2013
*** As Chronic Wasting Disease CWD rises in deer herd, what about risk for
humans?
Detection of PrPCWD in Rocky Mountain Elk Feces Using Protein Misfolding
Cyclic Amplification
Bruce E Pulford,1 Terry Spraker,1 Jenny Powers,2 Margaret Wild2 and Mark D.
Zabel1 1Department of Microbiology; Immunology and Pathology; College of
Veterinary Medicine and Biomedical Sciences; Colorado State University;
2Biological Resource Management Division; United States National Park Service;
CO, USA
Key words: CWD, feces, PMCA, elk
Chronic wasting disease (CWD) is a transmissible spongiform encephalopathy
affecting cervids, including mule and white-tailed deer (Odocoileus hemionus and
virginianus), elk (Cervus elaphus nelsoni) and moose (Alces alces shirasi). The
method of CWD transmission between hosts is unclear, though there is evidence
that feces excreted by infected animals may play a role. Recently, CWD prions
was detected in feces using bioassays in cervidized mice, which took many months
to produce results. In this study, we use a more rapid procedure, protein
misfolding cyclic amplification (PMCA), to test elk feces for the presence of
PK-resistant cervid PrP (PrPCWD). Feces were collected from symptomatic and
asymptomatic elk in several northern Colorado locations, homogenized, mixed with
normal brain homogenate from Tg5037 mice (expressing cervid PrP) and subjected
to up to 9 rounds of PMCA (1 round = 40 secs sonication/30 mins at 70% maximum
power, 24 hours). Western blots were used to detect PrPCWD using BAR-224
anti-PrP antibody. Rectal and CNS tissue from the elk were IHC-labeled and
examined for the presence of PrPCWD. Fecal samples from symptomatic and
asymptomatic elk that tested positive by IHC showed characteristic PrPCWD bands
on western blots following PMCA. In addition, PMCA detected PrPCWD in 25% of
fecal samples from IHC-negative animals. These data suggest that PMCA may (1)
prove useful as a non-invasive method to supplement or even replace IHC testing
of cervids for CWD, and (2) identify additional asymptomatic carriers of CWD,
the prevalence of which may be underestimated using IHC.
Detection of subclinical infection in deer orally exposed to urine and
feces (1) suggests that a prolonged subclinical state can exist, necessitating
observation periods in excess of two years to detect CWD infection, and (2)
illustrates the sensitive and specific application of sPMCA in the diagnosis of
low-level prion infection. Based on these results, it is possible that low doses
of prions, e.g. following oral exposure to urine and saliva of CWD-infected
deer, bypass significant amplification in the LRS, perhaps utilizing a neural
conduit between the alimentary tract and CNS, as has been demonstrated in some
other prion diseases.
In summary, we provide evidence for the presence of infectious prions in
the brains of conventional prion-assay-negative deer orally exposed 19 months
earlier to urine and feces from CWD-infected donor deer. This apparent low level
of prion infection was amplified by sPMCA, confirmed by Tg[CerPrP] mouse
bioassay, and detected only in the obex region of the brain. These results
demonstrate the potential for CWD prion transmission via urine and/or feces, and
highlight the application of more sensitive assays such as sPMCA in
identification of CWD infection, pathogenesis, and prevalence.
In contrast, CWD prions have been reported in saliva, urine and feces,
which are thought to be responsible for horizontal transmission. While the
titers of CWD prions have been measured in feces, levels in saliva or urine are
unknown. Because sheep produce ~17 L/day of saliva and scrapie prions are
present in tongue and salivary glands of infected sheep, we asked if scrapie
prions are shed in saliva. We inoculated transgenic (Tg) mice expressing ovine
prion protein, Tg(OvPrP) mice, with saliva from seven Cheviot sheep with
scrapie. Six of seven samples transmitted prions to Tg(OvPrP) mice with titers
of -0.5 to 1.7 log ID50 U/ml. Similarly, inoculation of saliva samples from two
mule deer with CWD transmitted prions to Tg(ElkPrP) mice with titers of -1.1 to
-0.4 log ID50 U/ml. Assuming similar shedding kinetics for salivary prions as
those for fecal prions of deer, we estimated the secreted salivary prion dose
over a 10-mo period to be as high as 8.4 log ID50 units for sheep and 7.0 log
ID50 units for deer. These estimates are similar to 7.9 log ID50 units of fecal
CWD prions for deer. Because saliva is mostly swallowed, salivary prions may
reinfect tissues of the gastrointestinal tract and contribute to fecal prion
shedding. Salivary prions shed into the environment provide an additional
mechanism for horizontal prion transmission.
Conclusions. This study documents the first aerosol transmission of CWD in
deer. These results further infer that aerosolized prions facilitate CWD
transmission with greater efficiency than does oral exposure to a larger prion
dose. Thus exposure via the respiratory mucosa may be significant in the facile
spread of CWD in deer and perhaps in prion transmission overall.
Conclusion. Transepithelial transport of prions across nasal cavity mucosa
begins within minutes of inhalation and can continue for up to 3 h. While M
cells appear to transport prions across the follicular associated epithelium,
larger amounts of prions are transported between the cells of the respiratory
and olfactory epithelia, where they immediately enter the lymphatic vessels in
the lamina propria. Thus, inhaled prions can be spread via lymph draining the
nasal cavity and have access to somatic and autonomic nerves in the lamina
propria of the nasal cavity. The increased efficiency of the nasal cavity route
of infection compared with the oral route may be due to the rapid and prolonged
transport of prions between cells of the respiratory and olfactory epithelia.
Now that these experiments are completed we conclude that TSE infectivity
is likely to survive burial for long periods of time with minimal loss of
infectivity and restricted movement from the site of burial. These experiments
emphasize that the environment is a viable reservoir for retaining large
quantities of TSE infectivity, and reinforce the importance of risk assessment
when disposing of this type of infectious material.
Friday, December 06, 2013 2:39 PM
Procedures for identifying infectious prions after passage through the
digestive system of an avian species
A CONTRIBUTION TO THE NEUROPATHOLOGY OF THE RED-NECKED OSTRICH (STRUTHIO
CAMELUS) - SPONGIFORM ENCEPHALOPATHY
4.21 Three cases of SE’s with an unknown infectious agent have been
reported in ostriches (Struthio Camellus) in two zoos in north west Germany
(Schoon @ Brunckhorst, 1999, Verh ber Erkeg Zootiere 33:309-314). These birds
showed protracted central nervous symptoms with ataxia, disturbances of balance
and uncoordinated feeding behaviour. The diet of these birds had included
poultry meat meal, some of which came from cattle emergency slaughter cases.
SE1806
TRANSMISSION STUDIES OF BSE TO DOMESTIC FOWL BY ORAL EXPOSURE TO BRAIN
HOMOGENATE
1 challenged cock bird was necropsied (41 months p.i.) following a period
of ataxia, tremor, limb abduction and other neurological signs.
Histopathological examination failed to reveal any significant lesions of the
central or peripheral nervous systems...
1 other challenged cock bird is also showing ataxia (43 months p.i.).
snip...
94/01.19/7.1
A notification of Spongiform Encephalopathy was introduced in October 1996
in respect of ungulates, poultry and any other animal.
4.23 MAFF have carried out their own transmission experiments with hens. In
these experiments, some of the chickens exposed to the BSE agent showed
neurological symptoms. However MAFF have not so far published details of the
symptoms seen in chickens. Examination of brains from these chickens did not
show the typical pathology seen in other SE’s. 4.24 A farmer in Kent in November
1996 noticed that one of his 20 free range hens, the oldest, aged about 30
months was having difficulty entering its den and appeared frightened and tended
to lose its balance when excited. Having previously experienced BSE cattle on
his farm, he took particular notice of the bird and continued to observe it over
the following weeks. It lost weight, its balance deteriorated and characteristic
tremors developed which were closely associated with the muscles required for
standing. In its attempts to maintain its balance it would claw the ground more
than usual and the ataxia progressively developed in the wings and legs, later
taking a typical form of paralysis with a clumsy involuntary jerky motion.
Violent tremors of the entire body, particularly the legs, became common,
sparked off by the slightest provocation. This is similar to that seen in many
BSE cases where any excitement may result in posterior ataxia, often with
dropping of the pelvis, kicking and a general nervousness. Three other farmers
and a bird breeder from the UK are known to have reported having hens with
similar symptoms. The bird breeder who has been exhibiting his birds for show
purposes for 20 years noticed birds having difficulty getting on to their perch
and holding there for any length of time without falling. Even though the bird
was eating normally, he noticed a weight loss of more than a pound in a bird the
original weight of which was 5 pounds. 4.25 Histological examination of the
brain revealed degenerative pathological changes in hens with a minimal
vacuolation. The presence of PrP immunostaining of the brain sections revealed
PrP-sc positive plaques and this must be regarded as very strong evidence to
demonstrate that the hens had been incubating Spongiform Encephalopathy.
OPINION on : NECROPHAGOUS BIRDS AS POSSIBLE TRANSMITTERS OF TSE/BSE ADOPTED
BY THE SCIENTIFIC STEERING COMMITTEE AT ITS MEETING OF 7-8 NOVEMBER 2002
OPINION
1. Necrophagous birds as possible transmitters of BSE. The SSC considers
that the evaluation of necrophagous birds as possible transmitters of BSE,
should theoretically be approached from a broader perspective of mammals and
birds which prey on, or are carrion eaters (scavengers) of mammalian species.
Thus, carnivorous and omnivorous mammals, birds of prey (vultures, falcons,
eagles, hawks etc.), carrion eating birds (crows, magpies etc.) in general could
be considered possible vectors of transmission and/or spread of TSE infectivity
in the environment. In view also of the occurrence of Chronic Wasting Disease
(CWD) in various deer species it should not be accepted that domestic cattle and
sheep are necessarily the only source of TSE agent exposure for carnivorous
species. While some information is available on the susceptibility of
wild/exotic/zoo animals to natural or experimental infection with certain TSE
agents, nothing is known of the possibility of occurrence of TSE in wild animal
populations, other than among the species of deer affected by CWD in the
USA.
1 The carrion birds are animals whose diet regularly or occasionally
includes the consumption of carcasses, including possibly TSE infected ruminant
carcasses.
C:\WINNT\Profiles\bredagi.000\Desktop\Necrophagous_OPINION_0209_FINAL.doc
snip...
skroll down to the bottom ;
Date: Mon, 11 Jun 2001 16:24:51 –0700
Reply-To: Bovine Spongiform Encephalopathy
Sender: Bovine Spongiform Encephalopathy
From: "Terry S. Singeltary Sr." Subject: The Red-Neck Ostrich & TSEs
'THE AUTOPSY'
see full text and more ;
Friday, February 25, 2011 Soil clay content underlies prion infection odds
UPDATED DATA ON 2ND CWD STRAIN
Wednesday, September 08, 2010
CWD PRION CONGRESS SEPTEMBER 8-11 2010
Spiroplasma spp. from transmissible spongiform encephalopathy brains or
ticks induce spongiform encephalopathy in ruminants
Frank O. Bastian1, Dearl E. Sanders2, Will A. Forbes2, Sue D. Hagius1, Joel
V. Walker1, William G. Henk3, Fred M. Enright1 and Philip H. Elzer1
also, see page 104 here ;
Identifying the role of different organs and organisms in scrapie
transmission
Prions can survive for years in soil but how can scrapie be transmitted? A
group of teams from France, Iceland and Spain is setting out to study the role
of nematode parasites, nasal fly, ticks and mites in the transmission process
and to determine to what extent wild rodents could serve as reservoir of prion.
It is also examining possible vertical transmission through embryo organs. This
work will permit a better understanding of the wide spread of scrapie in
naturally infected flocks, taking into account the genetic susceptibility of the
hosts.
Manech Blond-face sheep in the French Pyrenees and Latcha Blond-face in
Spain are breeds particularly susceptible to scrapie, but the disease occurs
only in some French flocks. A comparative survey between infected and
non-infected flocks with scrapie will be conducted to compare the infection with
parasites such as nematode worms, nasal fly and ticks. Wild rodent populations
will be compared as will be mites from fresh grass and hay. These mites will be
also studied in infected and non-infected farms in Iceland. Experiments on sheep
and mice will provide a better understanding of the role of nematodes. The PrPsc
protein will be investigated in these organisms, and mice inoculations are
projected to demonstrate the possibility of prion transmission.
also, see ;
Sunday, December 15, 2013
*** FDA PART 589 -- SUBSTANCES PROHIBITED FROM USE IN ANIMAL FOOD OR FEED
VIOLATIONS OFFICIAL ACTION INDICATED OAI UPDATE DECEMBER 2013 UPDATE
TSS
posted by Terry S. Singeltary Sr. at
11:43 AM
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